State Consumer Disputes Redressal Commission
Vikas Kumar Asthna vs Sahara Hosipatal on 25 July, 2022
Cause Title/Judgement-Entry STATE CONSUMER DISPUTES REDRESSAL COMMISSION, UP C-1 Vikrant Khand 1 (Near Shaheed Path), Gomti Nagar Lucknow-226010 Complaint Case No. CC/36/2015 ( Date of Filing : 16 Feb 2015 ) 1. Vikas Kumar Asthna Lucknow ...........Complainant(s) Versus 1. Sahara Hosipatal Lucknow ............Opp.Party(s) BEFORE: HON'BLE MR. Rajendra Singh PRESIDING MEMBER HON'BLE MR. Vikas Saxena JUDICIAL MEMBER PRESENT: Dated : 25 Jul 2022 Final Order / Judgement Reserved State Consumer Disputes Redressal Commission U.P. Lucknow. Complaint Case No.36 of 2015 1- Vikas Kumar Asthana aged about 56 years, S/o Late Shri Pyare Lal Asthana, M-2/838, Vinay Khand, Gomti Nagar, Lucknow-226010 (Uttar Pradesh) 2- Kavita Asthana, aged about 51 years, W/o Mr. Vikas Kumar Asthana, M-2/838, Vinay Khand, Gomti Nagar, Lucknow-226010 (Uttar Pradesh) ...Complainants. Versus 1- Sahara Hospital through its Managing Director, Office at Viraj Khand-1, Gomti Nagar, Lucknow 226010 (Uttar Pradesh) 2- Dr. Sandeep Agarwal, Senior Consultant, Neuro Medicine at Sahara Hospital, Viraj Khand-1, Gomti Nagar, Lucknow-226010 (Uttar Pradesh) 3- The New India Assurance Co. Ltd., 3rd Floor, Arif Chamber-I, Kapoorthala, Aliganj, Lucknow-226020. 3- The Oriental Insurance Co. Ltd., A 22/27, Asaf Ali Raod, New Delhi-110002. ...Opposite parties. Present:- 1- Hon'ble Sri Rajendra Singh, Member. 2- Hon'ble Sri Vikas Saxena, Member. Sri Sushil Kumar Sharma, Advocate for the complainants. Sri Alok Kumar Srivastava & Sri R.N. Singh, Advocates for Opposite Parties no.1 & 2. None for the opposite party no.3. Sri Anchal Mishra, Advocate for the Opposite party no.4 Date :30.08 .2022 JUDGMENT
Per Sri Rajendra Singh, Member- The brief facts of the complaint are that, that this case is being filed against the negligence, inadequate, deficient services provided by the opposite parties and negligent medical practice of the opposite parties during the treatment of late Urmila Asthana, the mother of the complainants. Late Smt. Urmila Asthana, aged about 78 years was a retired lecturer of Government Girls Inter College, Pratapgarh, U.P. She was hale and hearty. While enjoying her happy retired life on 16th June, 2014 night at about 10.45 p.m. her left side of the face became numb, drooped and her speech was slurred and she partially became unconscious. These were symptoms of brain stroke (i.e. Acute Ischemic Stroke) blockage of blood rupturing and preventing blood flow to the brain. The complainants took their mother immediately to Sahara Hospital, Lucknow where she was admitted on 17.6.2014 at 12.15 a.m. Under the instructions of the hospital the complainant deposited Rs.20,200.00. Thereafter, the junior doctor attended the patient. After an hour of admission, the complainants enquired about the health and situation of their mother. The attending doctor informed that there is nothing to worry about her. At 4.06 a.m. her C.T. Scan was done and the attending doctor stated that there is nothing serious and it is case of brain edema and the specialist doctor will attend the patient in the morning.
The senior specialist doctor Sandeep Agarwal (Neurologist)came in the morning and advised for MRI. On 17.6.2014 at 11.34 a.m., MRI was done. MRI report stated acute infarct (Rt) MCA territory making a diagnosis of acute stroke. Later on, the patient was shifted to Neuro Medicine Intensive Care Unit (NMICU). On 19.6.2014, when the complainants enquired about the health of his mother, Dr. Sandeep Agarwal stated that the patient is under the influence of medicines and assured that after 4 to 5 more days, the patient's condition will stabilize. On 23.6.2014, when the opposite party came for regular check-up, the condition of the patient was again enquired by the complainants. The opposite party stated that the patient's condition has improved as compared to past few days. Each and every time the complainants enquired about the health of the patient the opposite party assured him that the patient will recover but it is going to indefinite time. But on the flipside the condition of the patient kept deteriorating, this deterioration in health was clearly visible to every relative and people who visited the patient.
On 28.6.2014, the complainants spoke with the opposite party to know about the status of her mother's health. After examining the progress report, CT and MRI reports opposite party stated that nothing can be said about the health. He asked the complainants to shift his mother to semi private or private ward from NMICU. The administrator of Indoor Patient Day (IPD) met the complainants and asked him to shift his mother from NMICU as nothing could be said about the patient's recovery. Seeing no improvement in the medical condition of his mother, indecisiveness and incompetence in opposite party's behavior, the complainants shifted his mother back home on 1.7.2014. INR 2,01,200.00 were spent during the treatment at Sahara Hospital, Lucknow.
The complainant's mother breathed her last on 5.7.2014 at Ford Hospital, Gomti Nagar, Lucknow, as a result of cardiac and respiratory failure. After the funeral the complainants tried to understand the reason behind such sudden death of his mother. During the study of medical manuals available through internet, the complainant found that wrong treatment was given and administered by the opposite party. The complainants further studied about Acute Ischemic Stroke i.e. brain stroke, as the first MRI report stated acute infarct (Rt) MCA territory. As per medical thumb rule and according to brain stroke guidelines framed by United States, Food and Drug Administration and National Institute of Neurological and Strokes, it is case of serious medical emergency. Requisite medication should be provided within three (3) golden hours post stroke. It is prudent to mentionthat the treatment which laws given to the complainant's mother was obsolete and not closed to the structured advance treatment which is recommended by US-FDA and NINDS. According to the guidelines when a person has shown the symptoms of brain stroke and reached the nearby well equipped hospital well within three hours, they require immediate medical and radiological intervention in the form of DSA or Magnetic Resonance Angiography (MRA) and immediately thereafter RTPA infusion via DSA catherer or Hyperacute Thrombolysis with IV RTPA of acute ischemic stroke. If complications are dealt quickly, there is a good chance of recovery and correct treatment provided within three (3) golden hours can save life of the person.
MRI was conducted too late i.e. after crucial delay of thirteen (13) long hours. The patient was admitted to Sahara Hospital, Lucknow within one and half hours post brain stroke. The medical services provided by the opposite parties were inadequate and negligent. In cases of emergency and extreme situations like this, where there is crisis of time, CT/MRI should be performed immediately but in the given case the CT scan was performed after unnecessary delay of three long hours from the time patient reported to the hospital amounting to negligence in services. Post that DSA and thereafter, treatment of stroke by recombinant Tissue Plasminogen Activator (rtPA) or Hyperacute thrombolysis with IV rTPA or Acute Ischemic Stroke should have been administered on the patient but the same was never performed by the Sahara Hospital Lucknow. This Matter of fact of not providing the right treatment within requisite time was main cause of death of my mother and the same is attributed only because of utter negligence of doctors of Sahara Hospital, Lucknow.
By the time, Dr. Sandeep Agarwal started requisite treatment and medication, it was too late to recover a patient who has undergone Acute Ischemic Stroke. Pursuant to brain stroke guidelines framed by UD FDA and NINDS, it is a serious medical emergency and require medication should be provided within 3 hours after onset of the stroke symptoms. It is prudent to mention that the treatment which was given to my client's mother was obsolete and not close to the structured advance treatment which is recommended by US FDA & NINDA. When a person has shown the symptoms of brain stroke and reached the nearby well equipped hospital well within 3 hours they require immediate medical and radiological intervention in the form of DSA or Magnetic Resonance Angiography (MRA) and immediately thereafter rTPA infusion via DSA Catheter or IV Thrombolysis. If complications are dealt quickly, there is a good chance of recovery and correct treatment provided within 3 golden hours can save life of the person. Thepatient would have survived and have not succumbed to complete brain stroke. Even the ordinary skill, care and expertise were not practiced by Dr. Sandeep Agarwal.
The mother of the complainants was admitted in the hospital of the opposite parties and considerations for the hospitalization and expenses were born by the complainants. Therefore, the complainants are the consumers of the opposite parties under definition of section 2(d) of the Consumer Protection Act, 1986.Late Urmila Asthana, the mother of the complainants was admitted in the opposite partieshospital where the opposite parties offered negligent and inadequate services. Thus, as the provision of section 2(e) of the Act, 1986, the dispute has been arises and is continued till date. Thus, the present complaint case is within the time limitation as per Consumer Protection Act, 1986.
The complainants have prayed for refund of Rs.87,47,226.00 together with interest @ 18% p.a. from the date of death of their mother i.e. 5.6.2014 as per following details.
Pecuniary Damages/Liquidated Damages:
Direct cost associated with the victim, Urmila Asthana
1.
Loss of prospective future earnings of the deceased. She was an ex-state government employee and her late husband as also a State Government employee, both had a pensionable job.
She used to get a pension of INR 14,550.00 per month and also a family pension on behalf of her late husband Shri P.L. Asthana amounting to INR 11,950.00. total pension she use to withdraw was INR 26,500.00 per month.
Minimum life expectancy fifteen (15) years approximately from date she expired i.e. 5.7.2014.
INR 26,500 (per month pension* 15 years* 12 months = 47,70,000.00
2. Paid for treatment at Sahara Hospital/ Ford Hospital INR 1,92,136/-+ 20,000/- +2760/- +250/- +1760/-+200/-+10,120/-=2,27,226/-
Cost associated with Urmila Asthana's son Mr. Vikas Asthana
1. Funeral Expenses INR 1,00,000/-
2. Transportation expenses and other miscellaneous expenses due to hospitalization.
INR 75,000/-+25,000/- = 1,00,000/-
3. Loss of income for missed work.
INR 50,000/-
Total Pecuniary Damages INR 52,47,226/-
Non-pecuniary damages/un-liquidated damages:
1.
Loss of mother's companionship and and other life amenities.
INR 10,00,000/-
2. Emotional distress, pain and suffering for the entire family members.
INR 20,00,000/-
3. Pain/suffering endured by the victim during medical treatment.
INR 5,00,000/-
Total Non-pecuniary damages 35,00,000/-
Grand Total of damages (INR-52,47,226/- +35,00,000/-
87,47,226/-
The opposite parties have filed their written statement wherein it is submitted thatthe contends of the complaint are inconsistent with the record available and are herewith denied. Rest of the contents are also denied unless specifically admitted. The opposite parties take support of the plea taken in defense into which are supplementary to each other and thepresent written statement is being filed without any prejudice and be considered for all purposes in its entirety and not in piece meal. It is not disputed that the patient late Urmila Asthana had approached the opposite party no.1 on 17.6.2017 at about 12.21 a.m. with left side hemiparesis with right angle deviation of mouth with slight slurring of speech. On examination by the attending doctor the patient was drowsy, having supra nuclear 7th nerve palsy and weakness of left half of the body. She was a known case of hypertension for last 15 years with many drugs for control of hypertension. As per the condition of the patient the treatment was immediately started.
It is also submitted that the complainant left the hospital against the medical advice of the doctors and took the patient home (DOPR). It is also submitted that the complainant himself was contributory for the death of the patient and making false allegation to the respondents since he did follow the advice of the management and treatment which has no guarantee.
It is submitted that the facility of DSA and rTPA infusion via DSA Catheter is not available in our hospital, this procedure is available only in SGPGI, Lucknow. Even a dedicated stroke unit is not available in our hospital. Only Intra Venous Thrombolysis can be done in out hospital. To give Intra Venous Thrombolysis is on discretion of doctor; because we have to look for risk and benefit ratio, and oreover because Intra Venous Thrombolysis can cause fatal intra cranial haemorrhages. The patient was not considered for Intra Venous Thrombolysis because symptoms appear inthe patient while she was sleeping. Further the exact time of onset of stroke could not be assessed; as such Intra Venous Thrombolysis should be done within 03 hours of golden period. The patient having altered sensorium at the onset of symptom and clinical examination, it may be taken as that the stroke may have involved more than 1/3 of cerebral hemisphere which increases chances of Intra Cranial Haemorrhage. The increasing age chances of Intra Cranial Haemorrhage increases. And after the age of 80 years thrombolysis is contraindicated. The patient was having age more than 78 years at the time of admission. The complainant has made allegation that the patient died because thrombolysis was not done on time. It is pertinent to mention here that according to Harrison 18th Edition Vol:2 page 3272, it is clearly stated that there was no significant reduction in mortality in patient on rtPA (21% as placebo and 17% rTPA). It is not denied that thrombolysis is beneficial in treating stroke; but it is not a sure shot treatment, as there was significant 12% increased number of patient with minimal disability (32% on placebo and 40% rTPA) thus thrombolysis would have caused more harm in thepatient, as such the patient developed bleed in the infracted area later. The patient having sub kind of infarct takes months and even years to recover.
The complainants are not the consumers of the answering opposite parties. The present complaint is being filed against the provisions of section 12(1)(c) of the Consumer Protection Act, 1986. It is the complainant who has created a false story without any evidence and basis and has filed the present complaint to extort money from the opposite parties. It is wrong to say that due to negligence of opposite parties the mother of the complainant met her demise. The opposite parties did not cause any physical/ mental ailment or financial loss to the complainant.
In view of the aforementioned there is no negligence on part of the answering opposite parties no.1 & 2 even as made in the averment in the complaint. However, the opposite parties have purchased insurance policies no.42040011130 100000265 & 221113/48/2015/80 for a period 1.1.2014 to 31.12.2014 & 15.4.2014 to 14.4.2015 by which the New India Assurance Company and the Oriental Insurance Company Ltd. have agreed to indemnify the opposite parties no.1 & 2 against all the claims which may arise from the fault and services given by the opposite parties no.1 & 2 as such for any liability which may arise from the service, of the hospital and the concerning doctor. The liability of the same shall be discharged by the insurance company.
There is no deficiency in service or unfair trade practices or negligent act on the part of the opposite parties no.1 & 2. The present complaint is not maintainable and liable to be dismissed with cost.
We have heard the learned counsel for the complainants Sri Sushil Kumar Sharma, learned counsel for theopposite parties no 1 &2 SriAlok Kumar Srivastava & Sri R.N. Singh, learned counsel for theOpposite party no.4Sri Anchal Mishra . Service on opposite party no 3 has already been held sufficient on 28.07.2017 . We have also heard opposite party no 2 Dr Sandeep Agrawal in person.
We have perused the pleadings, evidence is and documents on record.
In the present case the matter rates to Stroke . Regarding MCA territory stroke it is better to go through the following article :-
The middle cerebral artery (MCA) is the most common artery involved in acute stroke. It branches directly from the internal carotid artery and consists of four main branches, M1, M2, M3, and M4. These vessels provide blood supply to parts of the frontal, temporal, and parietal lobes of the brain, as well as deeper structures including the caudate, internal capsule, and thalamus. This activity describes the presentation, evaluation, and management of middle cerebral artery strokes, and explains the role of the members of the interprofessional team in assessing, diagnosing, managing, and rehabilitating patients who suffer from this, and how to try to prevent a recurrence.
Objectives:
Identify the various potential etiologies of middle cerebral artery stroke.
Summarize the most important evaluations needed to diagnose a middle cerebral artery stroke.
Outline the differential diagnoses that must be considered if a patient presents with stroke-like symptoms but does not have a stroke.
Review how to address the modifiable risk factors for secondary stroke prevention after a stroke, and how the interprofessional team can be involved in improving the outcome and quality of life of a stroke patient.
Introduction The middle cerebral artery (MCA) is the most common artery involved in acute stroke. It branches directly from the internal carotid artery and consists of four main branches, M1, M2, M3, and M4. These vessels provide blood supply to parts of the frontal, temporal, and parietal lobes of the brain, as well as deeper structures, including the caudate, internal capsule, and thalamus. Its vast supply means that strokes involving the MCA territory can have a multitude of presenting symptoms, depending on which branches and structures are affected.
Etiology There are multiple risk factors for strokes, which can be divided into modifiable and nonmodifiable categories--many of the causes of hemorrhagic and ischemic stroke overlap. The nonmodifiable risk factors of each include age, sex, race, and genetics. The risk increases as you get older; the risk is higher in men at a younger age, but the risk of death is higher overall in women; and the risk is significantly greater in African Americans, and slightly higher in Hispanics and Native Americans as well, compared to whites.
Modifiable risk factors, including hypertension, smoking, obesity, alcohol consumption, and diet all contribute to both ischemic and hemorrhagic stroke. However, hyperlipidemia, physical inactivity, diabetes, and cardiac causes such as cardiomyopathy, heart failure, and atrial fibrillation, are risk factors for ischemic stroke but not hemorrhagic stroke.
The etiology of hemorrhagic stroke is most frequently hypertension, especially in developing countries where the burden of hypertension is unknown due to infrequent screening and diagnosis. Less frequently, hemorrhagic strokes can also be due to angiopathies, which can be diagnosed with a cerebral angiogram.
Ischemic stroke is frequently broken into several etiological categories, including atherosclerotic, cardioembolic, lacunar, and cryptogenic. However, ischemic stroke can also, at times, be due to more specific causes such as vasculitis, dissections, or genetic disorders. In the case of atherosclerotic disease, severe stenosis or thrombosis can be caused by cholesterol plaques, which can cause occlusions of vasculature or stenosis of vessels, blocking blood flow and leading to cerebral ischemia. Cardioembolic strokes can occur in the case of atrial fibrillation or, in younger individuals, a patent foramen ovale, particularly in the setting of deep vein thromboses. In both of these cases, clots can travel from the heart through the left ventricle into the aorta and lodge in the internal carotid artery (ICA) or its branches, most frequently the MCA. The smaller deeper vessels that are the culprits of lacunar infarcts, such as the lenticulostriate arteries, are more often affected by hypertension and diabetes than by thromboses.[2] Epidemiology Stroke is the fifth leading cause of death in the United States and the second leading cause of death worldwide. The overall prevalence of stroke in the U.S. is 2.6% in adults over 20 years old. Approximately 85% of these are ischemic strokes, and over half of all ischemic strokes occur in MCA territory.[3] The risk of stroke is higher in men than women when young and middle-aged, but overall, women have a higher risk of stroke than men over the course of a lifetime, with the risk for women being 20% to 21% versus 14% to 17% in men. The risk of stroke is also higher in Blacks and Hispanics than Whites. Over the last few decades, stroke occurrence and mortality have overall decreased in the United States and other high-income countries, but no change in frequency has been observed in middle or low-income countries. In addition, mortality due to stroke has increased in middle and low-income countries. This is likely related to the advancements made in secondary stroke prevention in higher-income countries.[4] History and Physical When patients present with under 24 hours of neurological symptoms, such as weakness, dizziness, numbness, issues with speech, or visual changes, they are managed in the form of a stroke alert or a code stroke. This is done because there is a specific protocol that has to be followed to quickly obtain the most important components of the history, perform the pertinent parts of the physical exam, and get the emergent laboratory studies and relevant imaging. The most important component to obtain in the history of these patients is their last known normal, which is when they were last seen or last felt that they were at their baseline. The reason this is so important is that it determines what options are available for their management. If their last known normal is within 4.5 hours of presentation, they are within the window for receiving IV tissue plasminogen activator (TPA); if it is within 24 hours, they are within the window for neurosurgical intervention. Other additional important components of the history include when the symptoms started, what they were, and if they have changed, improved, or worsened since their onset. Whether or not the patient has any contraindications to TPA also needs to be obtained quickly. This includes any history of intracranial hemorrhage, ischemic stroke within the past 3 months, any recent invasive surgical procedures or recent neurosurgical or spinal surgeries, a recent history of any kind of internal bleeding, use of anticoagulant medications if they have had recent blood draws or IV lines at noncompressible sites, and recent trauma or myocardial infarction. Other components of history that are useful to know are the patient's medical problems, as issues such as diabetes, hypertension, and hyperlipidemia all increase the risk of stroke.
The most important part of the physical exam to perform in an emergent fashion when there is a concern for a stroke is the National Institute of Health Stroke Scale. This scale is a standardized way of assessing stroke patients to remove subjectivity during their examination. This scale is particularly useful for identifying and localizing strokes involving the anterior circulation, such as the middle cerebral artery, based on the functions they assess. The components include sensation, strength, and coordination in all 4 extremities; production and comprehension of speech, including naming and repetition; visual fields; orientation to self and time; and symmetry and sensation of the face. Large MCA strokes are usually the easiest to recognize of all strokes, as they tend to present with the major deficits that one thinks of when thinking of a stroke, such as unilateral flaccidity, forced gaze deviation, visual field cuts, and, if in the dominant hemisphere, speech deficits. This scale is useful in predicting whether there will be findings on the diffusion-weighted MRI. When performing this exam, it is also important to note whether any abnormalities appreciated are chronic, such as residual deficits from previous strokes. In addition, it is necessary to check vital signs, particularly the patient's blood pressure as hypertension and hypotension can both be associated with neurological symptoms, and blood pressure must be under 180/110 prior to administration of IV TPA.
Evaluation There are two options for radiologic imaging in the setting of acute stroke - CT or MRI. Regardless of the route taken, it is necessary to obtain imaging without contrast as well as vascular imaging. The CT without contrast will assess for subacute to chronic strokes, any kind of hemorrhage, and hypodense signs that may indicate a large acute stroke. The MRI, particularly the DWI, will demonstrate the same things, as well as an acute stroke within minutes to hours. The next step is either a CT or MR angiogram of the head and neck with perfusion that images from the aorta up to the brain. The purpose of the angiogram is to assess for areas of stenosis or occlusions that may explain the symptoms. The purpose of the perfusion scan is to determine the extent of tissue that has already been damaged versus the extent that is at risk of damage, the core versus the penumbra. This determines whether or not the patient is a candidate for mechanical thrombectomy. The reason the neck is imaged is to include the internal carotid arteries down to the aorta to determine if these structures are involved. If the patient gets a CT and CT angiogram, they will eventually need an MRI as well.
There are several important laboratory studies to be performed. One is a coagulation panel, particularly in the setting of a patient on warfarin, as it is important to know the patient's INR and whether or not it was at a therapeutic level. Complete blood counts and basic metabolic panels should also be sent. A point of care blood glucose should be obtained on initial patient evaluation to assess if this may be contributing to the patient's symptoms. Hypoglycemia can mimic stroke and can be life-threatening if not recognized and treated promptly. More laboratory studies that need to be evaluated in patients with stroke are glycosylated hemoglobin levels and a lipid panel. This is because part of secondary stroke prevention involves optimizing these levels, which will be discussed later. Lastly, cardiac enzymes should be sent as well to assess for cardiac abnormalities.
After a stroke has been identified, the patient typically will need to get an EKG and a transthoracic echocardiogram, as well as telemetry monitoring, in order to determine whether there is an intracardiac thrombus or cardiac abnormality that may be the source of the patient's stroke. Some of these abnormalities that increase the risk of stroke include atrial fibrillation, a patent foramen ovale, or akinesis or hypokinesis of the cardiac walls. Assessment for a patent foramen ovale is typically indicated in patients of a young age or with recurrent strokes of unknown etiology. If a cardioembolic source is likely and these studies are all normal, the patient will likely get a transesophageal echocardiogram or cardiac MRI to get a better visualization of the left ventricle for a thrombus and the left atrial appendage for a thrombus, respectively. If these are still negative, the patient will likely get a Holter monitor on discharge, typically for 30 days, to see if any arrhythmia is captured.
Treatment / Management In the acute setting, the interventions for an MCA stroke are IV tissue plasminogen activator (TPA) and thrombectomy, if the patient qualifies. As mentioned above, the time of onset will determine if the patient qualifies for these interventions. For IV TPA, the last known normal has to be within 4.5 hours of the administration of the thrombolytic. For thrombectomy, the last known normal has to be within 24 hours of intervention.[10] Outside of this window, there is no abortive therapy, and further treatment is geared toward symptom management and secondary stroke prevention.[5] Symptoms that may need to be managed in the acute setting vary with the severity of the stroke and will be further discussed in the section addressing complications.
Secondary stroke prevention is aimed at modifiable risk factors, which were briefly addressed in the section on etiology. Modifiable risk factors include diabetes, hypertension, hyperlipidemia, and smoking. The first value that is addressed is glycosylated hemoglobin, which is used to measure the presence and severity of diabetes. In a stroke patient, the goal is less than 6.5%. This needs to be managed with appropriate diabetic medications, dietary modification, and close monitoring of blood glucose as well as frequent checks of glycosylated hemoglobin levels in those above or approaching this value. This should be checked approximately every three months.
Blood pressure is another important modifiable risk factor. In the first 24 hours after the last known well, there is a period of permissive hypertension to prevent further ischemic injury to tissue at risk in the setting of low cerebral perfusion pressure. If the patient does not receive IV TPA, the goal is less than 220/120 mmHg. If the patient does receive TPA, it is less than 185/105 mmHg in order to decrease the risk of hemorrhagic transformation. After these 24 hours, the goal drops to normotensive, less than 140/90 mmHg, for the patient's lifetime. It is important to adjust blood pressure medications accordingly, and for the patient to closely monitor their blood pressure at home.
In order to manage hyperlipidemia, the patient needs their lipid profile checked, the target of which is the level of low-density lipoprotein (LDL). The goal LDL in a patient who has had a stroke is less than 70. If it is not at goal, they need a high-intensity statin medication, typically atorvastatin or rosuvastatin. If they are already on this medication before the stroke, the dosage needs to be increased if they are not at goal. If they are already at the maximum dose, this needs to be continued as such, regardless of whether they are at goal or not. LDL needs to be closely monitored every few months, particularly if the patient is newly started on a statin or their dosage is changed, in order to monitor whether their cholesterol levels are responding appropriately.
Another important modifiable risk factor is smoking. It is necessary to emphasize the importance of smoking cessation to a patient who is an active smoker and has had a stroke.
The final piece in secondary stroke prevention, and possibly the most important, is addressing the need for an antiplatelet or anticoagulant. The appropriate medication varies with the presentation, previous medication, and stroke etiology. If the patient does not receive TPA and has an NIHSS score of less than 4, it is recommended to use dual antiplatelet therapy with aspirin, between 81 mg to 325 mg at the discretion of the physician, and clopidogrel 75 mg daily for 3 months. After these 3 months, the patient can be continued on monotherapy. If the NIHSS score is greater than 4, the recommendation is to load with aspirin. If they were already on aspirin 81 mg daily, their dosage might be increased to 325 mg, or they may be switched to clopidogrel 75mg daily.
If they are found to have an intracardiac thrombus or atrial fibrillation, or another reason for anticoagulation, such as a recent history of deep venous thrombosis (DVT), then they can be continued on anticoagulation, and there is no indication from a neurologic perspective for antiplatelets. Studies have indicated that there is no significant difference in stroke recurrence in the setting of holding anticoagulation versus resuming within 24 hours (48 if the patient receives IV TPA). However, some studies have indicated a slightly increased risk for hemorrhagic transformation if it is resumed in 48 hours up to 7 days. Typically, due to this difference in the risk of hemorrhagic transformation, it is recommended to hold anticoagulation in the immediate period following acute ischemic stroke.
Differential Diagnosis The differential diagnosis in a patient with stroke-like symptoms is extensive because there are a large number of stroke mimickers. A stroke must be ruled out in the acute setting as its management is highly time-sensitive. Once a stroke is ruled out, many other differentials must be considered. As described previously, MCA strokes typically present with the symptoms individuals associate most commonly with strokes, such as unilateral weakness and/or numbness, facial droop, and speech deficits ranging from mild dysarthria and mild aphasia to global aphasia.
Some dangerous central processes can be mistaken for stroke, such as subdural hematomas (SDH), intracranial hemorrhages (ICH), or masses, which also need to be recognized quickly. Masses, ICH, and SDH can cause stroke-like symptoms based on location or mass effect on the same structures in the brain that are supplied by the MCA. These may qualify for urgent surgical interventions, so it is important to identify these early. They would likely be diagnosed based on the CT or MRI that is performed in the acute setting when evaluating for stroke.
Seizures, particularly status epilepticus, can mimic stroke due to gaze deviation and loss of movement, as well as global aphasia due to loss of consciousness. This is important to diagnose acutely as well as it requires urgent treatment with benzodiazepines and antiepileptic drugs.
Demyelinating disorders such as multiple sclerosis may also be confused with stroke given presentations consistent with vision loss and numbness or weakness that typically will favor a particular extremity. This is something that will require an MRI with and without contrast to differentiate, as well as a thorough history and clarification of symptom onset, as it usually is not as acute and likely waxes and wanes.
Toxic, infectious, and metabolic differentials must be included as well, which is why several laboratory studies must be sent in the evaluation of acute stroke. Sepsis, uremia, hypo and hyperglycemia, hyponatremia, and hyperkalemia can all cause symptoms that resemble a stroke. Encephalopathic presentations due to these abnormalities and others can mimic stroke in that they can cause aphasia and apparent deficits in strength, which is why the assessment of laterality is so important in recognizing stroke versus some of its mimics. In these presentations, it can be more challenging to localize a possible central nervous system lesion as the deficits are usually more generalized. In these situations, in addition to the labs that are sent in the acute setting, there will need to be a more extensive laboratory workup, including an infectious workup.
Complex migraines can mimic stroke as well, as some migraines may present with unilateral weakness or numbness. This is something that imaging cannot help diagnose. Typically there will be a headache associated with the symptoms, and the patient will likely have a history of migraines and similar symptoms in the past. This is something that requires a thorough history to diagnose. Usually, treating the headache will result in symptom resolution.
Lastly, some psychiatric disorders may present with stroke-like symptoms, such as unilateral numbness or weakness. Examples of these are conversion disorder and panic attacks. These should be lower on the differential diagnosis, as other mimics need to be urgently diagnosed and treated, and can be dangerous and even fatal if misdiagnosed. These are typically diagnoses of exclusion and must be diagnosed based on a carefully obtained history.
Prognosis The prognosis of middle cerebral artery strokes depends on several factors. The most essential factors in determining prognosis are the size of the stroke, whether the patient received thrombolytic therapy and/or thrombectomy, and access to rehabilitation following the stroke. Explaining the prognosis after a stroke to the patients and their families can be challenging, particularly in the acute setting. It can take from weeks up to a year to reach a new baseline level of function. Patients who suffered smaller cortical strokes typically recover rapidly within a few weeks and then begin to level out over a few months. However, for larger strokes, it can be challenging to give a prognosis in even the first three months because the process of recovery varies so drastically between individuals. Mental status by day four usually can give the prognosis of the patient's mental status moving forward, but activities of daily living may take up to six months to establish a new baseline. Of note, physical therapy is as important in older patients as it is in younger patients in improving function.
In the case of severe MCA strokes, in which patients often battle cerebral edema and alteration of consciousness, mortality is frequently dependent upon whether life-saving measures are taken. Many patients qualify for tracheostomy and percutaneous gastrostomy tube placement, which increases the length of hospital stay and also increases the risk of infection. However, if they do not receive these interventions, their life expectancy is markedly decreased due to the inability to protect their airway or consume nutrients. In these patients, the prognosis is grim at best, the likelihood of recovery is very low, and their length of time of survival depends on whether or not these interventions are performed.
Complications There is an extensive number of complications that can occur following MCA stroke. Most stroke patients will develop some type of complication at some point during their recovery. According to one study of over 300 patients, 85% experienced at least one complication during their hospital stay alone, and most of the remaining individuals developed at least one complication within 6 weeks following their stroke. The patients were then followed over 30 months. The most common complications to occur in stroke patients while they are still hospitalized include infections, particularly pneumonia or urinary tract infections; falls; and pain. Less common complications include pressure sores, seizures, recurrent stroke, thromboembolism, and psychological complications, particularly depression. Following discharge and in the 30 months over which the patients were followed for this study, the most common complications continued to be infections, falls, and pain, but depression and anxiety also rose in prevalence. Concern for seizures and recurrent stroke persisted, and hospital readmission joined the list, while thromboembolism was only seen in one case.
The explanation as to why falls, pain, and infections are the most common complications has to do with the functions that MCA strokes impact most. Mobility is affected, particularly in the setting of decreased sensation and strength, which makes falls more likely to occur. Complications such as dysphagia can lead to aspiration, while decreased mobility can contribute to atelectasis, and both of these can promote the development of pneumonia. This decreased mobility is a large contributing factor to pressure sores and pain as well. This is why interdisciplinary teams are crucial in the recovery and improvement of quality of life of stroke patients.
Patients who suffer more severe strokes tend to suffer more dangerous and potentially fatal complications. These include cerebral edema, depression of consciousness, severe dysphagia, and inability to protect their airway. When cerebral edema occurs, which typically peaks around day 3 to 5 following acute stroke, this can put pressure on the ventricles and cause midline shift. If the patient does not have significant atrophy or just has very significant swelling, this can quickly progress to herniation and death. If it does not get to this point, it can still lead to severe depression of mental status, which can cause patients to be unable to protect their airway or swallow safely. This then leads to the difficult question of whether the patients should get tracheostomies or percutaneous gastric tubes placed, and these themselves can then lead to further complications and infections, while not getting these performed can lead to fatal outcomes as described previously in the section on prognosis.
Deterrence and Patient Education The primary education that is given to patients regarding strokes is risk factor modification for secondary stroke prevention and the warning signals for stroke, at which time they should call 911 and go to the nearest stroke center.
Secondary stroke prevention is implemented by addressing modifiable stroke risk factors, which include hypertension, hyperlipidemia, diabetes, diet, obesity, and smoking. Smoking cessation counseling is an important component of education, as is counseling regarding lifestyle and dietary modifications. Patients are typically started on aspirin if they had not been on it previously. Their cholesterol and glycosylated hemoglobin levels are closely monitored every few months, and if the patients have hyperlipidemia or diabetes, these are addressed with the appropriate medications. Patients are also advised to closely monitor their blood pressure with an at-home blood pressure cuff, and antihypertensive medications are adjusted accordingly.
As for alarm signs, the acronym FAST has been used for years, which is recently being replaced with BE FAST, which stands for balance, eyes, face, arms, speech, and time. This can be elaborated upon so that patients have a better picture of alarm symptoms and when to return to the emergency department. Balance indicates falling in one direction or dizziness; eyes include sudden unilateral loss of vision or sudden onset double vision; face indicates facial drooping; arms stand for arm weakness or loss of sensation; speech can have multiple meanings including slurring, word-finding difficulty, or difficulty getting words out; and time indicates that "time is brain" and the faster they get to an emergency department, the better.
Enhancing Healthcare Team Outcomes Without an interdisciplinary team involved in the care of a stroke patient, many aspects of care and needs of the patient and family may slip through the cracks. In addition, and most importantly, the team members, typically including stroke neurologists, nurses, care coordinators, physical, occupational, kinesiological, and speech therapists, and pharmacists, each address different concerns and needs, and all make important contributions when it comes to discharge planning and the future management of the patient after their hospitalization.
It is important to have stroke specialists on the team, which include a stroke neurologist, but also needs to include nurses and therapists who have been trained to care for stroke patients. This is important, so the patient gets the care that is tailored to them and their needs. Pharmacists are often on the teams as well. They are helpful when it comes to medication reconciliation, education of physicians and nurses regarding medication management, as well as education of the patient and their families. Pharmacists are also needed to assess what needs the patients will have on discharge, such as medication teaching or dose packs and pill containers. Other important members of the team, depending on the patient's functional status, may include chaplains, palliative care, and neuropsychologists. Therapists are necessary to assess and recommend needs on discharge, such as inpatient rehabilitation and homecare. The interdisciplinary team and their daily or bi-weekly rounds are important for the appropriate care and planning for patients. These individuals are important as each of them can address different needs of the patients, and are all involved in the inpatient care, including medications, treatments, assessment, therapies, and family education, as well as discharge planning, such as the best way to provide medications based on insurance, rehabilitation and home care needs, appropriate medications and physician follow up, and patient and family education.[7] Studies have demonstrated that a team-based approach with multiple phases including discussion of a plan, formulation of a written plan, and implementation of this plan via conferences and video chats between physicians, nurses, therapists, care coordinators, and administrators results in improved function without a change in hospital length of stay or rate of discharge. This improvement in function, which is the primary endpoint for stroke patients, supports the importance of communication between healthcare workers in making plans for their patients to manage them in the best way possible and provide the greatest opportunity for an improved quality of life.
Figure CT head RIght MCA Stroke. Contributed by Scott Dulebohn, MD Figure Fig 1. Anatomy of brain vascular territories. ACA: anterior cerebral artery; MCA: middle cerebral artery; PCA: posterior cerebral artery; AICA: anterior inferior cerebellar artery; PICA: posterior inferior cerebellar artery; SCA: superior cerebellar artery. Fig (more...) Figure Right MCA stroke. Bajaj, Divyansh& Agrawal, Ankit & Bajaj, Suryansh. (2018). Recreational Nitrous Oxide Abuse Causing Ischemic Stroke in a Young Patient: A Rare Case Report. Cureus. 10. 10.7759/cureus.3761.
Figure Left MCA territory infarction. Contributed by Sunil Munakomi, MD Figure Hemorrhagic transformation within the left MCA territory infarction seen on SWI MRI sequence. Contributed by Sunil Munakomi, MD References Navarro-Orozco D, Sánchez-Manso JC. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): Jul 26, 2021. Neuroanatomy, Middle Cerebral Artery. [PubMed]
2.Boehme AK, Esenwa C, Elkind MS. Stroke Risk Factors, Genetics, and Prevention. Circ Res. 2017 Feb 03;120(3):472-495. [PMC free article] [PubMed]
3. Ng YS, Stein J, Ning M, Black-Schaffer RM. Comparison of clinical characteristics and functional outcomes of ischemic stroke in different vascular territories. Stroke. 2007 Aug;38(8):2309-14. [PubMed]
4.Guzik A, Bushnell C. Stroke Epidemiology and Risk Factor Management. Continuum (MinneapMinn). 2017 Feb;23(1, Cerebrovascular Disease):15-39. [PubMed]
5.Arsava EM, Helenius J, Avery R, Sorgun MH, Kim GM, Pontes-Neto OM, Park KY, Rosand J, Vangel M, Ay H. Assessment of the Predictive Validity of Etiologic Stroke Classification. JAMA Neurol. 2017 Apr 01;74(4):419-426. [PMC free article] [PubMed]
6. Sartor EA, Albright K, Boehme AK, Morales MM, Shaban A, Grotta JC, Savitz SI, Martin-Schild S. The NIHSS Score and its Components can Predict Cortical Stroke. J Neurol Disord Stroke. 2013 Sep 13;2(1):1026. [PMC free article] [PubMed]
7.Boulanger JM, Lindsay MP, Gubitz G, Smith EE, Stotts G, Foley N, Bhogal S, Boyle K, Braun L, Goddard T, Heran M, Kanya-Forster N, Lang E, Lavoie P, McClelland M, O'Kelly C, Pageau P, Pettersen J, Purvis H, Shamy M, Tampieri D, vanAdel B, Verbeek R, Blacquiere D, Casaubon L, Ferguson D, Hegedus Y, Jacquin GJ, Kelly M, Kamal N, Linkewich B, Lum C, Mann B, Milot G, Newcommon N, Poirier P, Simpkin W, Snieder E, Trivedi A, Whelan R, Eustace M, Smitko E, Butcher K. Canadian Stroke Best Practice Recommendations for Acute Stroke Management: Prehospital, Emergency Department, and Acute Inpatient Stroke Care, 6th Edition, Update 2018. Int J Stroke. 2018 Dec;13(9):949-984. [PubMed]
8.Yaghi S, Herber C, Boehme AK, Andrews H, Willey JZ, Rostanski SK, Siket M, Jayaraman MV, McTaggart RA, Furie KL, Marshall RS, Lazar RM, Boden-Albala B. The Association between Diffusion MRI-Defined Infarct Volume and NIHSS Score in Patients with Minor Acute Stroke. J Neuroimaging. 2017 Jul;27(4):388-391. [PMC free article] [PubMed]
9.Ustrell X, Pellisé A. Cardiac workup of ischemic stroke. CurrCardiol Rev. 2010 Aug;6(3):175-83. [PMC free article] [PubMed]
10.Nogueira RG, Jadhav AP, Haussen DC, Bonafe A, Budzik RF, Bhuva P, Yavagal DR, Ribo M, Cognard C, Hanel RA, Sila CA, Hassan AE, Millan M, Levy EI, Mitchell P, Chen M, English JD, Shah QA, Silver FL, Pereira VM, Mehta BP, Baxter BW, Abraham MG, Cardona P, Veznedaroglu E, Hellinger FR, Feng L, Kirmani JF, Lopes DK, Jankowitz BT, Frankel MR, Costalat V, Vora NA, Yoo AJ, Malik AM, Furlan AJ, Rubiera M, Aghaebrahim A, Olivot JM, Tekle WG, Shields R, Graves T, Lewis RJ, Smith WS, Liebeskind DS, Saver JL, Jovin TG., DAWN Trial Investigators. Thrombectomy 6 to 24 Hours after Stroke with a Mismatch between Deficit and Infarct. N Engl J Med. 2018 Jan 04;378(1):11-21. [PubMed]
11.Johnston SC, Easton JD, Farrant M, Barsan W, Conwit RA, Elm JJ, Kim AS, Lindblad AS, Palesch YY., Clinical Research Collaboration, Neurological Emergencies Treatment Trials Network, and the POINT Investigators. Clopidogrel and Aspirin in Acute Ischemic Stroke and High-Risk TIA. N Engl J Med. 2018 Jul 19;379(3):215-225. [PMC free article] [PubMed]
12.Core A, Pinner N, Bethea B, Starr JA. Timing of Anticoagulation in Atrial Fibrillation Status Post Cardioembolic Stroke. J Pharm Pract. 2020 Oct;33(5):612-617. [PubMed]
13.Smythe MA, Parker D, Garwood CL, Cuker A, Messé SR. Timing of Initiation of Oral Anticoagulation after Acute Ischemic Stroke in Patients with Atrial Fibrillation. Pharmacotherapy. 2020 Jan;40(1):55-71. [PubMed]
14.Hosseininezhad M, Sohrabnejad R. Stroke mimics in patients with clinical signs of stroke. Caspian J Intern Med. 2017 Summer;8(3):213-216. [PMC free article] [PubMed]
15.Seitz RJ, Donnan GA. Recovery Potential After Acute Stroke. Front Neurol. 2015;6:238. [PMC free article] [PubMed]
16.Walcott BP, Miller JC, Kwon CS, Sheth SA, Hiller M, Cronin CA, Schwamm LH, Simard JM, Kahle KT, Kimberly WT, Sheth KN. Outcomes in severe middle cerebral artery ischemic stroke. Neurocrit Care. 2014 Aug;21(1):20-6. [PMC free article] [PubMed]
17.Langhorne P, Stott DJ, Robertson L, MacDonald J, Jones L, McAlpine C, Dick F, Taylor GS, Murray G. Medical complications after stroke: a multicenter study. Stroke. 2000 Jun;31(6):1223-9. [PubMed]
18. Aroor S, Singh R, Goldstein LB. BE-FAST (Balance, Eyes, Face, Arm, Speech, Time): Reducing the Proportion of Strokes Missed Using the FAST Mnemonic. Stroke. 2017 Feb;48(2):479-481. [PubMed]
19.Strasser DC, Falconer JA, Stevens AB, Uomoto JM, Herrin J, Bowen SE, Burridge AB. Team training and stroke rehabilitation outcomes: a cluster randomized trial. Arch Phys Med Rehabil. 2008 Jan;89(1):10-5. [PubMed] Differentiating between Hemorrhagic Infarct and Parenchymal Intracerebral Hemorrhage P. M. C. Choi, 1 J. V. Ly, 1 V. Srikanth, 1 H. Ma, 1 W. Chong, 2 M. Holt, 2 and T. G. Phan 1 ,* Author information Article notes Copyright and License information Disclaimer This article has been cited by other articles in PMC.
Abstract Differentiating hemorrhagic infarct from parenchymal intracerebral hemorrhage can be difficult. The immediate and long-term management of the two conditions are different and hence the importance of accurate diagnosis. Using a series of intracerebral hemorrhage cases presented to our stroke unit, we aim to highlight the clues that may be helpful in distinguishing the two entities. The main clue to the presence of hemorrhagic infarct on computed tomography scan is the topographic distribution of the stroke. Additional imaging modalities such as computed tomography angiogram, perfusion, and magnetic resonance imaging may provide additional information in differentiating hemorrhagic infarct from primary hemorrhages.
1. Introduction In acute stroke, the differential diagnosis of hemorrhage detected on computed tomography (CT) scan ranges from hemorrhagic infarct (HI), primary intracerebral hemorrhage (ICH) to hemorrhage from venous infarction. The differentiation between the first two conditions can be difficult, and there are currently no radiological criteria to assist in this regard. It is, therefore, not surprising that previous investigators have found poor agreement in making a diagnosis of HI or ICH.
HI, or hemorrhagic transformation of an infarct, occurs in approximately one-third of cases of ischaemic stroke [3]. When an infarct is immediately followed by the occurrence of petechial hemorrhage in the same arterial territory, the diagnosis of HI is easily made. However, when brain imaging is delayed after the onset of the patient's stroke symptoms, an erroneous diagnosis of ICH may be made if the hemorrhage appears confluent on CT. This issue of misdiagnosing HI has been recently raised by other investigators and may also be partly responsible for the overestimation of the prevalence of ICH [4]. Correct assignment of diagnosis is critical in guiding both acute and long-term management and also estimating prognosis. Patients with ischaemic stroke are more likely to develop recurrent ischaemic stroke than ICH. Antiplatelet is the mainstay therapy for this group of patients. Likewise, the finding of HI and atrial fibrillation suggests that the stroke mechanism is cardioembolism and anticoagulation needs to be considered. Furthermore, it has also been suggested that some cases of "ICH" in patients on anticoagulants may in fact be HI and thus represent "failure of anticoagulation" rather than anticoagulant-induced ICH.
2. Clinical Factors and Mechanism of HI HI occurs more commonly in elderly patients and those with larger infarcts. Among patients receiving thrombolytic therapy, it occurs more commonly in patients with diabetes and hypertension. It has also been associated with carotid endarterectomy and carotid artery stenting.
HI typically happens within 1-2 weeks after stroke onset, less commonly (~9%) in the first 24 hours. The occurrence of dense hematoma complicating HI may be even lower at approximately 3%. The mechanism of HI has been postulated to be due to breakdown of the basal lamina of microvessels related to activity of matrix metalloproteinase. This may be a consequence of prolonged ischaemia and exacerbated by recanalisation of the occluded artery. It has been suggested that tissue plasminogen activator (tPA) may exacerbate this process, but spontaneous intrainfarct hematoma can also occur in the absence of thrombolysis.
3. Recognition of HI on CT Scans A classification of HI based on the topography and intensity of hemorrhage on CT has previously been proposed by Moulin et al. in 1993 [1]: type 1, a multifocal or pethechial hemorrhagic infarction and type 2, an intra-infarct hematoma. The appearance of the latter can mimic ICH on CT scans. Careful observation of the deep structures involved by the stroke lesion and the topography of the surrounding hypodensity may help in reaching the correct diagnosis.
ICH involving the caudate nucleus is uncommon (Figures (Figures11 and and2)and involvement of both the caudate nucleus and putamen may suggest embolism affecting the lenticulostriate arteries and hemorrhagic infarction of the striatocapsular region (Figures (Figures3,3, ,4,4, and and5). Petechial hemorrhage after intravenous thrombolysis is easily recognized given there is always a baseline CT scan done prior to thrombolysis. The initial CT scan may also show coexisting signs of ischaemia such as the hyperdense middle cerebral artery (MCA) sign and the loss of insula ribbon (Figure 6).
Figure 1 75-year-old woman presented with left hemiparesis and headache. (a) Axial unenhanced CT images show a deep right thalamic hemorrhage (arrow) sparing the caudate nucleus. (b) Cerebral blood flow images show an area of decreased flow matching the area of the hematoma. There are no underlying features to suggest that this is a hemorrhagic infarct.
Figure 2 67-year-old man presented with left-sided hemiparesis. (a) Axial unenhanced CT images 2 hours after stroke show a hematoma lateral to the right lentiform nucleus with minimal surrounding hypodensity (arrow). The caudate nucleus is spared. (b) Similar to Figure 1, there is an area of decreased cerebral blood flow in the area of the hematoma. The overall picture is consistent with intracerebral hemorrhage.
Figure 3 74-year-old woman presented with right hemiparesis lasting few minutes but ongoing residual sensory deficits. (a) Initial axial unenhanced CT images show an old left frontal infarct only. (b) 12 hours after her initial symptoms, she developed recurrent right hemiparesis and aphasia. Repeated axial-unenhanced CT images show obscuration and loss of grey white differentiation in the left lentiform nucleus (thick arrow) and a dense left middle cerebral artery (thin arrow). (c) Axial unenhanced CT images 24 hours after stroke show a large left parenchymal hematoma within the striatocapsular region. Importantly, even in the absence of the previous CT studies, the involvement of the caudate head in the last series of CT images raises the possibility of hemorrhagic infarct. Stage IIH d2.
Figure 4 55-year-old man presented with dense left hemiparesis one week after right carotid stenting. (a) Initial axial unenhanced CT shows a large area of low attenuation in the right middle cerebral artery territory. (b) axial DW-MR image 2 hours later confirms a large infarct in the striatocapsular region, including the right caudate head. (c) Axial unenhanced CT 12 hours later shows a large parenchyma hemorrhage within the wedge-shaped area of infarction, consistent with hemorrhagic transformation. The case demonstrates two features typical of hemorrhagic infarct: the involvement of the caudate head and the distribution of the oedema surrounding the stroke lesion following the affected arterial territory. Stage IIH d2 [1].
Figure 5 69-year-old man with atrial fibrillation on warfarin, he presented with a 2-day history of left hemiparesis and neglect. (a) Initial axial unenhanced CT images show hemorrhage in the right basal ganglia, involving the right caudate head, unusual for ICH. Stage IIH d1 [1]. Warfarin was stopped and anticoagulation was reversed. (b) Axial unenhanced CT images 10 days later show further extension of hematoma with the surrounding hypodensity extending out to the cortex. (c) Axial unenhanced CT images 1 month after stroke show an extensive area of hypoattenuation in the right MCA territory. There is also an area of low attenuation more posteriorly (thin arrow), not evident on the previous CT and separate from the initial stroke, raising the possibility of a new subacute infarct since the first stroke. (d) Axial T2-weighted MR images 3 months after stroke show the posterior temporal infarct evident on the last CT scan more clearly, suggestive of bland infarction in that region. The cessation of warfarin after the first stroke probably contributed to this cardioembolic stroke. (e) On reviewing the initial CT images, a dense right middle cerebral artery sign is present on the coronal view (but not axial), further suggesting the first stroke is a hemorrhagic infarct rather than a hemorrhagic stroke.
Figure 6 82-year-old man presented with left hemiparesis. (a) Axial unenhanced CT images 2 hours after stroke show a hyperdense right MCA (thick arrow) and loss of the insular ribbon (thin arrow). Patient received intravenous thrombolysis after the CT. (b) Axial unenhanced CT images 3 days later show petechial hemorrhages in the striatocapsular area and a hematoma within the right lentiform nucleus, consistent with hemorrhagic transformation after thrombolysis. Stage HI d1 [1]. (c) CT perfusion image shows a large area of delayed mean transit time on the right. (d) CT angiogram shows truncation of mid M1 segment of the right middle cerebral artery (arrow).
The hypodense region of oedema surrounding the hematoma in ICH usually radiate centripetally, and it does not follow the topography of an arterial territory. Similar pattern of oedema is seen in hemorrhages resulting from venous infarction (Figures (Figures7 and and8).. In patients with HI, the hypodense regions surrounding the hematoma may reach the cortical surface and spread far from the centre of the hematoma (Figures (Figures9,,10,, and and11).. The topography of this hypodense region usually follows the affected vascular territory. Maps of the MCA and the posterior cerebral artery (PCA) infarct territory have been recently published and can be used to aid assignment of territorial membership of the stroke. The centre of the hematoma in cases of HI seems to correspond to regions at highest risk of infarction on the infarct map. For example, in the MCA territory, the region at risk is the striatocapsular region and in the PCA territory, the medial temporal and occipital lobes.
Figure 7 43-year-old woman presented with acute confusion with no history of trauma. (a) Axial unenhanced CT images show a large hemorrhage centered in the left temporal lobe. The subtle hyperdensity in the left sigmoid sinus is suggestive of thrombus (arrow). The topography of the lesion is not what would be expected from a hemorrhagic infarct involving the inferior division of the middle cerebral artery, that is, the surrounding hypodensity fails to reach the cortical surface. (b) MR venogram shows occlusion of the left transverse and sigmoid sinuses, confirming the hemorrhage is secondary to venous infarction.
Figure 8 57-year-old woman presented with dysphasia, headache, and vomiting. Axial unenhanced CT images show hemorrhage in the left temporal parietal area. Apart from the typical temporal location suggesting this may be a venous hemorrhage, there is also high attenuation in the left sigmoid sinus (arrowhead), left transverse sinus (thin arrow), and straight sinus (thick arrow). MR venogram confirms occlusion of these sinuses (not shown).
Figure 9 78-year-old man presented with right hemiparesis and dysphasia. (a) Axial unenhanced CT images 5 hours after stroke show an area of low attenuation in the left lentiform nucleus. (b) Repeated axial unenhanced CT images 3 days later show a parenchymal hematoma within the area of infarct. Stage HI d2. Even if the initial CT images are not available, the topography of the stroke is suspicious for hemorrhagic infarct. The centre of the hematoma is in the striatocapsular region with the surrounding hypodensity extending superiorly, following the topography of the middle cerebral artery.
Figure 10 75-year-old man presented with slurred speech. (a) Axial unenhanced CT images show an acute left parietal hemorrhage. The hypodense area around the hemorrhage reaches superiorly and out to the cortical surface, following the middle cerebral artery territory. Stage HI c2. (b) Axial fluid-attenuated inversion recovery MR sequences confirm the area of infarction reaching the surface of the cortex, suggesting that the stroke is a hemorrhagic infarct.
Figure 11 83-year-old man with atrial fibrillation, he presented with left-sided weakness and neglect. (a) Axial unenhanced CT images within 3 hours of symptom onset show no acute changes. (b) Axial unenhanced CT images 10 days after stroke show a hemorrhage within a wedge-shaped infarct in the right posterior parietal lobe. The surrounding hypodense area follows the topography of the middle cerebral artery, reaching out to the cortex and superiorly, consistent with a hemorrhagic infarct. Stage HI c2.
4. MR Imaging Features of HI The magnetic resonance (MR) imaging features of HI on diffusion weighted imaging (DWI) sequence have a mixed appearance. Within the hemorrhagic area, the appearance between HI and ICH is indistinguishable. However, the presence of an ischaemic process may be evidenced by discrete regions of restricted diffusion remote from the hemorrhagic area (Figures (Figures12-14). These lesions further strengthen the possibility of the primary lesion being a HI.
Figure 12 60-year-old man presented with dysphasia and confusion for 2 days. (a) Axial unenhanced CT images show a left frontal hematoma with surrounding hypodensity spreading from the centre, reaching superiorly and out to the cortical surface. The shape and topography of the lesion suggest that the primary event is an infarct, with secondary hemorrhagic transformation. Stage HI c2 [1]. (b) Axial diffusion weight MR images show 2 small discrete lesions within the left parietal and temporal lobes, suggesting concurrent infarcts in the same arterial territory. This further supports that the initial lesion is a hemorrhagic infarct, probably embolic in nature.
Figure 14 24-year-old woman presented with dense right hemiparesis and seizure. (a) Initial axial diffusion weighted MR images show an extensive area of diffusion restriction in the left basal ganglia and insular cortex. There is also a small area of restricted diffusion in the left corona radiate (arrow). Staphylococcus was grown from her peripheral blood culture, and she was treated for bacterial endocarditis. (b) Axial unenhanced CT images 3 weeks later show extensive hemorrhage within the area of the initial infarction. Stage IIH d2. (c) MR angiogram shows occlusion of the left middle cerebral artery, consistent with hemorrhagic transformation of the initial stroke.
Time-of-flight MR angiography can show the presence of occlusive intracranial disease and hence aids in confirming the diagnosis of HI (Figures (Figures13--14). Although not widely available, MR perfusion imaging may help in diagnosing HI if it shows the presence of a perfusion deficit extending beyond the region of hematoma. In ICH, the region of perfusion deficit does not extend beyond the ICH.
Figure 13 54-year-old man with a history of idiopathic thrombocytopenic purpura presented with acute coronary syndrome. He developed a dense right hemiparesis overnight. (a) Initial axial unenhanced CT images show a large left "fronto-temporal hemorrhage", initially thought to be secondary to his low platelet count of 20. Stage IIH c2 [1]. (b) Axial diffusion weighted MR images reveal areas of restricted diffusion remote from the area of hemorrhage (arrow heads). (c) The areas of diffusion weighted abnormality have low apparent diffusion coefficient values (arrows). (d) Digital probabilistic maps of middle cerebral artery territory infarcts show both the infarcts and hemorrhage lie within the middle cerebral artery territory. (e) Coronal unenhanced images from the original CT show a dense left internal carotid artery in the cavernous sinus (thin arrow). (f) MR angiogram confirms occlusion of the left internal carotid middle cerebral arteries. The overall picture suggests that the stroke is a HI.
The presence of "microbleeds" on gradient-echo (GRE) or susceptibility weighted imaging (SWI) sequence suggests the presence of blood product but does not necessarily indicate that the lesion in question is HI or ICH. In elderly patients, it has been recognised that some patients with ischaemic stroke may also have evidence of silent microbleeds. Lobar ICH tend to be located posteriorly, corresponding to the distribution of microbleeds and the location of binding of amyloid tracer in PET studies.
5. Role of CT Angiography and Perfusion CT angiography (CTA) is often used as a screening tool to exclude the possibility of aneurysmal bleed. It can also be used to concurrently evaluate the possibility of arterial occlusion and potential intra-arterial therapy. Given the additional risk of radiation exposure and iodinated contrast agents, further studies are required to evaluate the usefulness of this modality for determining arterial occlusion in patients with isolated putaminal or thalamic hemorrhage.
CT perfusion (CTP) with cerebral blood flow, cerebral blood volume, and mean transit time is usually performed at the same time as CTA in tertiary stroke centres. When this is available, it can help with differentiation between HI and ICH. In contrast to ischaemic stroke, a large perfusion defect around an ICH has not yet been reported. The presence of such a mismatch may point to the possibility of HI.
6. Conclusion Differentiating HI from ICH can be difficult. Careful examination of the topography of the stroke on the initial CT in different sections may distinguish the two conditions. Signs compatible with an infarct such as dense artery sign and insular ribbon sign should be actively looked for. Advanced imaging technique such as CTA, CTP, and MR imaging may be particularly helpful in difficult cases, looking for perfusion deficit, arterial occlusion, and diffusion restriction remote from the site of hemorrhages. Distinguishing HI from ICH is important given the difference in acute and long term management.
References
1. Moulin T, Crepin-Leblond T, Chopard JL, Bogousslavsky J. Hemorrhagic infarcts. European Neurology. 1993;34(2):64-77. [PubMed] [Google Scholar]
2. Lovelock CE, Rothwell PM, Anslow P, et al. Substantial observer variability in the differentiation between primary intracerebral hemorrhage and hemorrhagic transformation of infarction on ct brain imaging. Stroke. 2009;40(12):3763-3767. [PubMed] [Google Scholar]
3. Hart RG, Easton JD. Hemorrhagic infarcts. Stroke. 1986;17(4):586-589. [PubMed] [Google Scholar]
4. Bogousslavsky J, Regli F, Uske A, Maeder P. Early spontaneous hematoma in cerebral infarct: is primary cerebral hemorrhage overdiagnosed? Neurology. 1991;41(6):837-840. [PubMed] [Google Scholar]
5. Bailey RD, Hart RG, Benavente O, Pearce LA. Recurrent brain hemorrhage is more frequent than ischemic stroke after intracranial hemorrhage. Neurology. 2001;56(6):773-777. [PubMed] [Google Scholar]
6. Paciaroni M, Agnelli G, Corea F, et al. Early hemorrhagic transformation of brain infarction: rate, predictive factors, and influence on clinical outcome: results of a prospective multicenter study. Stroke. 2008;39(8):2249-2256. [PubMed] [Google Scholar]
7. Gilligan AK, Markus R, Read S, et al. Baseline blood pressure but not early computed tomography changes predicts major hemorrhage after streptokinase in acute ischemic stroke. Stroke. 2002;33(9):2236-2242. [PubMed] [Google Scholar]
8. Demchuk AM, Morgenstern LB, Krieger DW, et al. Serum glucose level and diabetes predict tissue plasminogen activator- related intracerebral hemorrhage in acute ischemic stroke. Stroke. 1999;30(1):34-39. [PubMed] [Google Scholar]
9. Henderson RD, Phan TG, Piepgras DG, Wijdicks EFM. Mechanisms of intracerebral hemorrhage after carotid endarterectomy. Journal of Neurosurgery. 2001;95(6):964-969. [PubMed] [Google Scholar]
10. Hamann GF, Okada Y, Fitridge R, Del Zoppo GJ, Povlishock JT. Microvascular basal lamina antigens disappear during cerebral ischemia and reperfusion. Stroke. 1995;26(11):2120-2126. [PubMed] [Google Scholar]
11. del Zoppo GJ, von Kummer R, Hamann GF. Ischaemic damage of brain microvessels: inherent risks for thrombolytic treatment in stroke. Journal of Neurology Neurosurgery and Psychiatry. 1998;65(1):1-9. [PMC free article] [PubMed] [Google Scholar]
12. Chung CS, Caplan LR, Yamamoto Y, et al. Striatocapsular hemorrhage. Brain. 2000;123, part 9:1850-1862. [PubMed] [Google Scholar]
13. Kumral E, Evyapan D, Balkir K. Acute caudate vascular lesions. Stroke. 1999;30(1):100-108. [PubMed] [Google Scholar]
14. Phan TG, Donnan GA, Wright PM, Reutens DC. A digital map of middle cerebral artery infarcts associated with middle cerebral artery trunk and branch occlusion. Stroke. 2005;36(5):986-991. [PubMed] [Google Scholar]
15. Phan TG, Fong AC, Donnan G, Reutens DC. Digital map of posterior cerebral artery infarcts associated with posterior cerebral artery trunk and branch occlusion. Stroke. 2007;38(6):1805-1811. [PubMed] [Google Scholar]
16. Schellinger PD, Fiebach JB, Hoffmann K, et al. Stroke MRI in intracerebral hemorrhage: is there a perihemorrhagic penumbra? Stroke. 2003;34(7):1674-1679. [PubMed] [Google Scholar]
17. Koennecke HC. Cerebral microbleeds on MRI: prevalence, associations, and potential clinical implications. Neurology. 2006;66(2):165-171. [PubMed] [Google Scholar]
18. Ly JV, Donnan GA, Villemagne VL, et al. 11C-PIB binding is increased in patients with cerebral amyloid angiopathy-related hemorrhage. Neurology. 2010;74(6):487-493. [PubMed] [Google Scholar] Now we have come to the facts of the case. The opposite parties have stated that there is no facility of DSA and Rtpa infusion via DSA catheter in the hospital and this procedure is only available in SGPGI . They further admitted that even a dedicated stroke unit is not available in the hospital. Only intravenous thrombolysis can be done in the hospital. Now the question arises that when the main facility was not available in the hospital why did they not refer the patient to SGPGI ?
A minority of stroke patients is eligible for thrombolytic therapy. Small pilot case series have hinted that elevation of incident arterial blood pressure might be associated with a favorable prognosis either in acute or subacute stroke. However, these patients were not considered for thrombolytic therapy and were not followed - up systematically. We used pharmacologically induced hypertension in a stroke patient with middle cerebral artery (MCA) occlusion ineligible for thrombolysis that was followed-up by radiological, clinical and functional outcome assessment.
Case presentation A patient with acute embolic MCA occlusion producing a large, ischemic penumbra confirmed by perfusion CT was treated by induced hypertension with phenylephrine started within 4 h of admission. Increase in the mean arterial pressure by 20% led to a reduction of neurological deficit by 3 points on the National Institute of Stroke Scale. MRI and CT scans performed during phenylephrine infusion showed the presence of limited subcortical and cortical infarct changes that were clearly less extensive than the perfusion deficit in the brain perfusion CT at baseline, found in the absence of MCA patency. No complications due to induced hypertension therapy occurred. Moderate functional improvement up to modified Rankin scale 2 at follow up took place.
Conclusion Induced hypertension in acute ischemic stroke seems clinically feasible and may be beneficial in selected normo- or hypotensive stroke patients not eligible for thrombolytic recanalization therapy.
Background Blood pressure (BP) increases after the first minutes of acute cerebrovascular occlusion and decreases significantly from admission to 12 hours after thrombolysis especially in case of adequate recanalization. The physiologic reasons for BP elevation, presumably may represent increased sympathetic autonomic nervous activity mediated by cerebral reticular neuronal networks and the medullary vasomotor center that regulate the tone of resistance of vessels of the body. Due to the failure of auto-regulation of cerebral blood flow (CBF) in the ischemic human brain, the CBF is passively dependent on the mean arterial pressure. Thus, the acutely elevated BP may help to maintain a vital level of CBF to support the existing penumbra, and contribute to the preservation of neurological function. Therefore, hypertension may be a risk marker of poor outcome due to initially large infarction or failed vessel recanalization rather than a causative factor of the acute ischemic stroke.
Induced hypertension (IH) is a standard treatment for cerebral ischemia in patients with vasospasm after subarachnoidal hemorrhage. Elevation of BP may improve neurological function and CBF in subacute ischemic stroke [5], or alleviate the degree of neurologic dysfunction during acute ischemic stroke [6]. Phenylephrine-induced hypertension (PHE-IH) decreased perfusion deficit by 40% as detected by MRI on the next day [7], suggesting the efficacy of PHE-IH in precluding infarct maturation within the ischemic penumbra.
We report a case where thrombolysis of acute embolic MCA occlusion was not possible due to undocumented onset time of stroke symptoms, but where a large area of cerebral cortex corresponding to ischemic penumbra did not undergo infarction following IH therapy.
Case presentation A 72-year right-handed woman with paroxysmal atrial fibrillation (AF), hypertension, coronary artery disease (CAD), asthma and 2 recent transient ischemic attacks was admitted to the emergency department with left hemiparesis and dysarthria that were noticed on awakening 4 h 30 min prior to the admission. She had no anticoagulant therapy. The baseline Barthel index of activities of daily living was 95 and Rankin scale (mRS) was 1. Neurologic examination revealed mild disorientation, left sensomotor hemiparesis, dysarthria, and visual and tactile neglect. The National Institute of Health Stroke Scale (NIHSS) score was 14. The mean BP was 150/72 mmHg, the mean MAP (mean arterial pressure) was 98 mmHg and ECG showed AF.
Immediate brain CT showed a hyperdense right MCA, hypoattenuation of the right lentiform nucleus and insular cortex as well as slight swelling of cortical sulci in the right frontoparietal region. Standard noncontrast CT scanning was performed with a Lightspeed Ultra CT scanner (General Electric Medical Systems; Version 05 MW 14.5.H2_P_M8_G) using the following parameters: 140 kV (posterior fossa/infratentorial)/120 kV (supratentorial), automatic mA (80-150 mA), 512 × 512 image matrix, 23-cm displayed field of view (DFOV), and 5-mm (posterior fossa/infratentorial)/7,5-mm (supratentorial) slice thickness.
In CT perfusion examination, the flow- and mean transit time images showed a broad perfusion deficit in the right MCA region. The blood volume chart, however, showed a clearly less significant defect in this region, consistent with the presence of large ischemic penumbra in the cortical cerebral tissue within the MCA territory (Fig (Fig1,1, top row). CT angiography documented a thrombus of 1 cm in length in the right MCA. Some signs of blood flow were detected distally in the right MCA, presumably resulting from collateral circulation (not shown). For the perfusion CT study, 4 adjacent levels were selected at the level of the basal nuclei. Fifty 5-mm CT sections of continuous (cine) scanning (80 kV, 200 mA) were obtained at every adjacent level, with a total acquisition time of 50 seconds. Computed tomography was initiated 5 seconds after the intravenous rapid infusion (injection rate of 7 ml/s) of 350 mg/ml iodinated nonionic contrast material (Iomeron 350, Bracco). The contrast agent was injected into an antecubital vein with a power injector (Medrad).
Figure 1 Mean MAP on admission, during induced hypertension (days 1-5) and tapering off (days 6-7).
A diagnosis of a cardio-embolic right MCA occlusion was thus established. Due to the delay in admission and uncertain timing of symptom onset the patient was not eligible for thrombolysis. In attempt to salvage the obviously large ischemic penumbra, induced hypertension (IH) therapy by phenylephrine (PHE) (Neo-Synephrine 0,1 mg/ml; initial dose 0.5 mg/hour)) and crystalloids 3000 ml/day intravenously was initiated 4 hours after the admission. The goal of 20 % MAP augmentation was achieved within 1 hour after the initiation of the PHE-infusion (Figure (Figure1).1). During the next 4 days the average MAP was maintained at 120 (range 140-91) mmHg with PHE infusion rate up to 3,5 mg/hour, thereafter PHE was tapered off during 2 days (average MAP 114,5 (range 133-99) mmHg). During PHE infusion the patient had paroxysmal AF with average heart rate 100 beats/min. The antihypertensive medication (Athenolol and Lozartan) that the patient had before the admission was stopped at the time of initiation of IH.
Four hours after the initiation of MAP augmentation the gaze deviation and the left leg weakness were improved and NIHSS was 12. Sixteen hours after the MAP augmentation the left facial weakness and hemiparesis were improved, although the patient was still slightly somnolent, and had moderate dysarthria and neglect. The NIHSS improved to 11. The brain CT and MRI scans performed 21 h and 26 h after admission showed the presence of a limited subcortical infarct on the distal region of the right lentiform nucleus and corona radiata. There were only subtle signs of a cortical infarction. Moreover, the extent of the subcortical infarct was substantially smaller than that of the perfusion deficit found in the brain perfusion CT on admission (Fig. (Fig.2,2, bottom row). MRA showed the persistence of the right MCA occlusion (Fig. (Fig.2,2, middle row).
Figure 2 Top row, left: Admission CT showing hypoattenuation of the right lentiform nucleus and insular cortex as well as slight swelling of cortical sulci in the right frontoparietal region. Top row, the third and the fourth pictures: The perfusion CT on admission, with flow and mean transit time CT showing a broad perfusion deficit in the right MCA region. Top row, the second picture: The volume chart shows only a small deficit in the right MCA region, consistent with the presence of a large ischemic penumbra in the cortical cerebral tissue. Middle row: The follow-up brain MRI showing the presence of a limited subcortical infarct on the distal region of the right lentiform nucleus and corona radiata. Signs of only a subtle cortical infarction are seen. From left to right: FLAIR MRI, T2-diffusion-weighted MRI, apparent diffusion coefficient. Middle row, right: The persistence of the right MCA occlusion on the follow up MRA. Bottom row: Day 2 CT showed that the extent of the subcortical infarct was substantially smaller than that of the perfusion deficit found in the CT perfusion brain scan obtained on admission.
During the following days the patient experienced a mild improvement on her level of alertness and in the left hemiparesis, with less significant improvement in the severity of dysarthria and neglect. Antithrombotic treatment with sodium daltreparin followed by warfarin was instituted. When discharged to the rehabilitation hospital, the patient had a NIHSS of 7. At the 3-month control visit she was independent in main activities of daily living, but needed a walking device when strolling outside. The uncontrasted control brain CT showed the previous right MCA infarct without any new signs of ischemia (not shown). NIHSS was 4; Barthel index was 80 and mRS 3. At 10-month interview she lived at home and walked independently, Barthel index was 90 and mRS 2.
Conclusion Many stroke patients are not eligible for thrombolysis due to delay in the admission or unclear timing of symptom onset. Still, there may be a therapeutic window for salvaging of brain tissue through improvement of CBF in the ischemic penumbra, which seems to exist well beyond the sofar approved 3-hour window.
This case study suggests the potential utility of IH in the treatment of acute stroke beyond the conventional thrombolytic treatment window. Studies have documented the existence of an ischemic penumbra up to 24 hours after stroke onset the and therapeutic time window for salvaging brain tissue may be substantially longer .
Sparing of the ischemic penumbral brain tissue in the present case was confirmed by the follow-up MRI and supported by the relatively good functional outcome. The spontaneous clot lysis or sudden improvement of collaterals to the occluded MCA territory seems unlikely because the original vascular occlusion as well as collateral flow remained essentially identical on the follow-up MRA. A degree of functional improvement was achieved already acutely upon increasing the average MAP by 20%.
Although we cannot confirm that it was PHE-IH that was crucially responsible for the diversion toward a benign outcome, our past experience of nonrecanalized acute MCA occlusions in elderly patients attests of a much more extensive infarct maturation in the MCA territory, especially in cases where BP drops during the first night following the admission. In accordance with previous reports of using IH [9] this study demonstrates relative safety of PHE- IH, the patient was closely monitored, and no evidence of cardiac ischemia were seen, the chest x ray did not reveal any signs of pulmonary edema, and no hemorrhagic transformation on CT scans was observed.
In conclusion, PHE-IH seems to be feasible and could be beneficial in selected stroke patients within 6 hours from stroke symptom onset. A prospective, randomized study of PHE-IH could be warranted to examine whether PHE-IH can salvage ischemic brain tissue in acute, documented cerebrovascular occlusions that are not amenable for thrombolytic therapy even though ischemic penumbra still exists.
Now let us see the oath taken be a doctor before entering the nobel profession of the Medical World. As per guidelines of MCI, Every member should get it framed in his or her office it should never be violated in its letter and spirit.
"I solemnly pledge myself to consecrate my life to service of humanity.
Even under threat, I will not use my medical knowledge contrary to the laws of Humanity.
I will maintain the utmost respect for human life from the time of conception.
I will not permit considerations of religion, nationality, race, party politics or social standing to intervene between my duty and my patient.
I will practice my profession with conscience and dignity.
The health of my patient will be my first consideration.
I will respect the secrets which are confined in me.
I will give to my teachers the respect and gratitude which is their due.
I will maintain by all means in my power, the honour and noble traditions of medical profession.
I will treat my colleagues with all respect and dignity.
I shall abide by the code of medical ethics as enunciated in the Indian Medical Council (Professional Conduct, Etiquette and Ethics) Regulations 2002.
I make these promises solemnly, freely and upon my honour."
The complexity of the human body and the uncertainty involved in the medical procedure are of such great magnitude that it is impossible for a Doctor to guarantee a successful result; and the only assurance that he can give, or can be understood to have given by implication is that he is possessed of requisite skill in that branch of profession which he is practising and while undertaking the performance of the task entrusted to him, he would be exercising his skills with reasonable competence. An ordinary physician or surgeon is not expected to be either a clodhopper or feckless practitioner of profession, as much as, he is not expected to be a paragon, combining qualities of polymath or prophet as in the realm of diagnosis and treatment, there is ample scope for genuine difference of opinion; and a Doctor cannot be treated as negligent merely because his conclusion differs from that of other persons in the profession, or because he has displayed less skill or knowledge than others would have shown. The true test for establishing negligence in diagnosis or treatment on the part of a doctor is whether he has been proved to be guilty of such failure as no doctor of ordinary skill would be guilty of, if acting with ordinary care. Furthermore, a golden principle of law has been laid down by the Hon'ble Apex Court in Jacob Mathew Vs. State of Punjab, (AIR 2005 SC 3180) that no sensible professional would intentionally commit an act or omission which would result in loss or injury to the patient as the professional reputation of the person is at stake. A single failure may cost him dear in his career. Even in civil jurisdiction, the rule of res ipsa loquitor is not an universal application and has to be applied with extreme care and caution to the cases of professional negligence and in particular that of the doctors, else it would be counter productive. Simply because a patient has not favourably responded to a treatment given by a physician or a surgery has failed, the doctor cannot be held liable per-se by applying the doctrine of res ipsa loquitor. Yet, another golden principle of law has been laid down by the Hon'ble Apex Court in Indian Medical Association Vs. V.P. Santha's III (1995) CPJ 1 (SC) at para 37 that "it is no doubt true that sometimes complicated questions requiring recording of evidence of experts may arise in a complaint about deficiency in service based on the ground of negligence in rendering medical services by a medical practitioner; but this would not be so in all complaints about deficiency rendering services by a medical practitioner. There may be cases which do not raise such complicated questions and the deficiency in service may be due to obvious faults which can be easily established such as removal of the wrong limb or the performance of an operation on the wrong patient or giving injection of a drug to which the patient is allergic without looking into the out patient card containing the warning or use of wrong gas during the course of an anaesthetic or leaving inside the patient swabs or other items of operating equipment after surgery. Furthermore, it has been observed in Malay Kumar Ganguli's case (AIR 2010 SC 1162) that" charge of professional negligence on a medical person is a serious one as it affects his professional statusand reputation and as such, the burden of proof would be more onerous. A doctor cannot be held negligent only because something has gone wrong. He also cannot be held liable for mischance or misadventure or for an error in judgment in making a choice when two options are available. The mistake in diagnosis is not necessarily a negligent diagnosis." In the instant matter, thus a simple test, in the light of aforesaid observations, needs to be conducted in order to ascertain whether the Doctor is guilty of any tortious act of negligence/battery amounting to deficiency in conducting a surgery in the delivery of child and not properly attending the patient, the complainant and consequently, liable to pay damages for leaving cotton mass in the abdomen / stomach due to failure in surgery and deteriorating condition of the patient.
Now, it is required to be seen whether an expert report is necessary in each and every case relating to medical negligence or not ? It has been observed by the Hon'ble Apex Court in Indian Medical Association Vs. V.P. Santha III (1995) CPJ 1 (SC) at para 37 that "it is no doubt true that sometimes complicated questions requiring recording of evidence of experts may arise in a complaint about deficiency in service based on the ground of negligence in rendering medical services by a medical practitioner; but this would not be so in all complaints about deficiency rendering services by a medical practitioner. There may be cases which do not raise such complicated questions and the deficiency in service may be due to obvious faults which can be easily established such as removal of the wrong limb or the performance of an operation on the wrong patient or giving injection of a drug to which the patient is allergic without looking into the out patient card containing the warning or use of wrong gas during the course of an anaesthetic or leaving inside the patient swabs or other items of operating equipment after surgery. Furthermore, in B. Krishna Rao Vs. Nikhil Super Speciality Hospital 2010 (V) SCC513 at para 40 the Hon'ble Apex Court was pleased to hold that it is not necessary to have opinion of the expert in each and every case of medical negligence. The Hon'ble Apex Court was pleased to further hold in Nizam Institute of Medical Sciences Vs. Prashant S. Dhananka and others 2009 (VI) SCC 1 that "in a case of medical negligence, once initial burden has been discharged by the complainant by making of a case of negligence on the part of the hospital or the doctor concerned, the owner then shifts on the hospital or to the attending doctors and it is for the hospital to satisfy the court that there was no lack of care or diligence".
A doctrine or rule of evidence in tort law that permits an inference or presumption that a defendant was negligent in an accident injuring the plaintiff on the basis of circumstantial evidence if the accident was of a kind that does not ordinarily occur in the absence of negligencea plaintiff who establishes the elements of res ipsa loquitur can withstand a motion for summary judgment and reach the jury without direct proof of negligence-- Cox v. May Dept. Store Co., 903 P.2d 1119 (1995).
In Byrne vs Boadle, this maxim was used for the first time where the complainant was injured by a barrel that dropped from the window of the defendant. In the abovementioned case, Pollock, C. B., said "here are many incidents from which no presumption of negligence can arise, but this is not true in every case. It is the duty of persons who keep barrels in a warehouse to take care that they do not roll out and I think that such a case will, beyond all doubt, afford prima facie proof of negligence."
This doctrine intends to help direct the court proceedings to a conclusion, especially if it is established through the implication of this doctrine's rule that the injury caused to the claimant would not have occurred or taken place if the defendant wasn't negligent.This also gives enough cause and evidence to hold the defendant liable for his negligent actions.
The thing speaks for itselfis the gist of the maxim Res Ipsa Loquitur Maxim. What are the essentials of this maxim.
The injury caused to the plaintiff shall be a result of an act of negligence.
There is a lack of evidence, or the evidence presented before the court is insufficient to establish the possibilities of the fault of the plaintiff or third party.
The defendant owes a duty of care towards the plaintiff, which he has breached.
There is a significant degree of injury caused to the plaintiff.
Applicability of Doctrine of Res Ipsa Loquitur.
The maxim of res ipsa loquitur came into force to benefit the plaintiff as he can use circumstantial evidence to establish negligence.
Consequently, it shifts the burden of proof on the defendant, logic being, where there is an event of unexplained cause, usually, the one that does not occur without the defendant's negligence in controlling the action which has caused the injury to the claimant or destroyed his goods.
In this scenario, the court shall presume negligence on the part of the defendant in such a case unless it includes an appropriate explanation compatible with his taking reasonable care.
In AchutraoHaribhauKhodwa and Others vs. State of Maharashtra and Others, it was considered that the maxim should not be applied in the case of general incidences of neglect and shall only be reflected when there is a significant degree of injury caused.
Section 106 of the Indian Evidence Act Section 106 of the Act provides that when any fact is especially within the knowledge of any person, the burden of proving that fact is upon him.
Res ipsa loquitur is a Latin phrase that means "the thing speaks for itself." In personal injury law, the concept of res ipsa loquitur (or just "res ipsa" for short) operates as an evidentiary rule that allows plaintiffs to establish a rebuttable presumption of negligence on the part of the defendant through the use of circumstantial evidence.
This means that while plaintiffs typically have to prove that the defendant acted with a negligent state of mind, through res ipsa loquitur, if the plaintiff puts forth certain circumstantial facts, it becomes the defendant's burden to prove he or she was not negligent.
Res Ipsa Loquitur and Evidence Law Accidents happen all the time, and the mere fact that an accident has occurred doesn't necessarily mean that someone's negligence caused it. In order to prove negligence in a personal injury lawsuit, a plaintiff must present evidence to demonstrate that the defendant's negligence resulted in the plaintiff's injury. Sometimes, direct evidence of the defendant's negligence doesn't exist, but plaintiffs can still use circumstantial evidence in order to establish negligence.
Circumstantial evidence consists of facts that point to negligence as a logical conclusion rather than demonstrating it outright. This allows judges and juries to infer negligence based on the totality of the circumstances and the shared knowledge that arises out of human experience. Res ipsa is one type of circumstantial evidence that allows a reasonable fact finder to determine that the defendant's negligence caused an unusual event that subsequently caused injury to the plaintiff.
This doctrine arose out of a case where the plaintiff suffered injuries from a falling barrel of flour while walking by a warehouse. At the trial, the plaintiff's attorney argued that the facts spoke for themselves and demonstrated the warehouse's negligence since no other explanation could account for the cause of the plaintiff's injuries.
As it has developed since then, res ipsa allows judges and juries to apply common sense to a situation in order to determine whether or not the defendant acted negligently.
Since the laws of personal injury and evidence are determined at the state level, the law regarding res ipsa loquitur varies slightly between states. That said, a general consensus has emerged, and most states follow one basic formulation of res ipsa.
Under this model for res ipsa, there are three requirements that the plaintiff must meet before a jury can infer that the defendant's negligence caused the harm in question:
The event doesn't normally occur unless someone has acted negligently;
The evidence rules out the possibility that the actions of the plaintiff or a third party caused the injury; and The type of negligence in question falls with the scope of the defendant's duty to the plaintiff.
As mentioned above, not all accidents occur because of someone else's negligence. Some accidents, on the other hand, almost never occur unless someone has acted negligently.
Going back to the old case of the falling flour-barrel, it's a piece of shared human knowledge that things don't generally fall out of warehouse windows unless someone hasn't taken care to block the window or hasn't ensured that items on the warehouse floor are properly stored. When something does fall out of a warehouse window, the law will assume that it happened because someone was negligent.The second component of a res ipsa case hinges on whether the defendant carries sole responsibility for the injury. If the plaintiff can't prove by a preponderance of the evidence that the defendant's negligence cause the injury, then they will not be able to recover under res ipsa.
States sometimes examine whether the defendant had exclusive control over the specific instrumentality that caused the accident in order to determine if the defendant's negligence caused the injury. For example, if a surgeon leaves a sponge inside the body of a patient, a jury can infer that the surgeon's negligence caused the injury since he had exclusive control over the sponges during the operation.
In addition to the first two elements, the defendant must also owe a duty of care to protect the plaintiff from the type of injury at issue in the suit. If the defendant does not have such a duty, or if the type of injury doesn't fall within the scope of that duty, then there is no liability.
For example, in many states, landowners don't owe trespassers any duty to protect them against certain types of dangers on their property. Thus, even if a trespasser suffers an injury that was caused by the defendant's action or inaction and that wouldn't normally occur in the absence of negligence, res ipsa loquitur won't establish negligence since the landowner never had any responsibility to prevent injury to the trespasser in the first place.
Res ipsa only allows plaintiffs to establish the inference of the defendant's negligence, not to prove the negligence completely. Defendants can still rebut the presumption of negligence that res ipsa creates by refuting one of the elements listed above.
For example, the defendant could prove by a preponderance of the evidence that the injury could occur even if reasonable care took place to prevent it. An earthquake could shake an item loose and it could fall out of the warehouse window, for instance.
A defendant could also demonstrate that the plaintiff's own negligence contributed to the injury. To go back to the flour-barrel example, if the defendant shows that the plaintiff was standing in an area marked as dangerous it could rebut the presumption of negligence created by res ipsa.
Finally, the defendant could establish that he did not owe the plaintiff a duty of care under the law, or that the injury did not fall within the scope of the duty owed. For example, if the law only imposes a limited duty on the defendant not to behave recklessly, then res ipsa will not help the plaintiff by creating an inference of negligence since a negligent action would not violate the duty owed to the plaintiff.
According to the Blacks Law Dictionary the maxim is defined as the doctrine providing that, in some circumstances, the mere fact of accidents occurrence raises an inference of negligence so as to establish a prima facie (at first sight) case. It is a symbol for that rule that the fact of the occurrence of an injury taken with the surrounding circumstances may permit an inference or recipes omission of negligence, or make out a plaintiff's prima facie case and present a question of fact for defendant to meet with and explanation. It is merely a short way of saying that the circumstances attendant on the accident are of such a nature to justify a jury in light of common sense and past experience in inferring that the accident was probably the result of the defendant's negligence, in the absence of explanation or other evidence which the jury believes.
Its use in clinical negligence gained some traction before Bolam and Bolitho. Mahon v Osborne [1939] 1 All ER 535, is an early example of the application of res ipsa loquitur in a case where a surgical swab had been left inside a patient's body.
In Clarke v Worboys (1952) Times, 18 March, CA, a patient noticed burns on her buttock shortly after surgical excision of a breast tumour. The surgery involved cauterisation. The Court of Appeal held that this was a case where res ipsa loquitur applied. The outcome was not one that would ordinarily occur in the absence of negligence, and the surgical team were unable to explain how the injury was caused.
In Cassidy v Ministry of Health [1951] 2 KB 343, Denning LJ succinctly summarised the maxim's application to clinical negligence cases: "I went into hospital to be cured of two stiff fingers. I have come out with four stiff fingers and my hand is useless. That should not happen if due care had been used. Explain it if you can."
Ng Chun Pui Vs Lee Chuen Tat, the first defendant was driving a coach owned by the second defendant westwards in the outer lane of dual carriageway in Hong Kong. Suddenly the course across the central reservation and collided with a public bus travelling in the inner lane of the other carriageway, killing one passenger in the bus and injuring the driver and three others on the bus. The plaintiff could not prove that the defendants were negligent and had caused the accident. They however proceeded on the basis of Res Ipsa Loquitur and shifted the onus on the defendants to prove that they were not negligent. However, they failed to do so. And the judicial committee of the Privy Council held the defendants liable for the plaintiffs injuries. { MarkLuney and Ken Opliphant, Tort Law Text And Materials (Oxford University Press, New York, 2000) pp 173-175 } In A.S. Mittal &Anr Vs State Of UP &Ors , AIR 1979 SC 1570 , the defendants had organised an eye camp at Khurja along with the Lions Club. 88 low risk cataract operations were undertaken during the period of the camp. It was however, disastrous as many of those who had been operated upon lost their eyesight due to post medical treatment. Proceedings against the government initiated for negligence of the doctors. Damages worth Rs.12,500/- were paid as interim belief to each of the aggrieved. The decision was on the basis of Res Ipsa Loquitur as the injury would not ave occurred had the doctors not been negligent in not having followed up with post-operation treatment. Res Ipsa Loquitur can be applied in matters where are the procedures have not been followed and is not just limited to the commission of an act.
We can define 'Medical negligence' as the improper or unskilled treatment of a patient by a medical practitioner. This includes negligence in taking care from a nurse, physician, surgeon, pharmacist, or any other medical practitioner. Medical negligenceleads to 'Medical malpractices' where the victims suffer some sort of injury from the treatment given by a doctor or any other medical practitioner or health care professional.
Medical negligence can occur in different ways. Generally, it occurs when a medical professional deviates from the standard of care that is required.
So, we can say that any kind of deviation from the accepted standards of medication and care is considered to be medical negligence and if it causes injury to a patient then the doctor who operated on him, other staff and/or hospital may be held liable for this.
Some of the common categories of medical negligence are as follows:
Wrong diagnosis - When someone goes to a hospital, clinic or medical room, etc. the first step after admittance is the diagnosis. Diagnosing symptoms correctly is critical and important to provide medical care to any patient. However, if a patient is not treated properly due to any mistake in diagnosis, the doctor can be made liable for any further injury or damages caused as a result of the wrong diagnosis.
Delay in diagnosis - A delayed diagnosis is treated as medical negligence if another doctor would have reasonably diagnosed the same condition in a timely fashion. A delay in diagnosis can cause undue injury to the patient if the illness or injury is left to worsen with time rather than being treated. Obviously, any delay in the identification and treatment of an injury can reduce the chance of recovery for the patient.
Error in surgery - Surgical operations require an enormous level of skill and it should be done with due care and caution because even the slightest mistakes can have profound effects on the patient. The wrong-site surgery, lacerations of any internal organ, severe blood loss, or a foreign object being left in the body of the patients, all this comes under Surgical error.
Unnecessary surgery - Unnecessary surgery is usually associated with the misdiagnosis of patient symptoms or a medical decision without proper consideration of other options or risks. Alternatively, sometimes surgery is chosen over conventional treatments for their expediency and ease compared to other alternatives.
Errors in the administration of anesthesia - Anesthesia is a risky part of any major medical operation and requires a specialist (anesthesiologist) to administer and monitor its effect on the patient. Prior to any medical procedure requiring anesthesia, the anesthesiologist has to review the patient's condition, history, medications, etc. to determine the most suitable of all the medicine to use. Anesthesia malpractice can happen even during the pre-operation medical review or during the procedure itself.
Childbirth and labor malpractice - Childbirth is a difficult event for a woman and it becomes worse if not handled properly by the doctors and nurses. There are many instances of medical negligence during childbirth including the mishandling of a difficult birth, complications with induced labor, misdiagnosis of a newborn medical condition, etc. Long-Term negligent treatment - Medical negligence can also occur in subtle ways over the course of a long treatment period. Usually, the negligence can take the shape of a failure to follow up with treatment, or a doctor's failure to monitor the effects of the treatment properly.
A standard of care specifies the appropriate treatment and medication procedure as per the requirements that should be taken into account by a doctor while providing the treatment to his patients. The care should not be of the highest degree nor the lowest.Here, the degree means the level of care an ordinary health care professional, with the same training and experience, would render in similar circumstances in the same community. This is the critical question in medical malpractice cases and if the answer is "no," and you suffered injury as a result of the poor treatment, you may file a suit for medical malpractice.
In the case of Dr. Laxman Balkrishna Joshi Vs. Dr. TrimbakBapu Godbole and Anr.[ 1969 AIR 128], the Supreme Court held that a doctor has certain aforesaid duties and a breach of any of those duties can make him liable for medical negligence. A doctor is required to exercise a reasonable degree of care that is set for this profession.
Dr. Kunal Saha vs Dr. Sukumar Mukherjee on 21 October, 2011 ( NC) original petition number 240 OF 1999 is one of the most important case regarding medical negligence. The brief facts of the case are-
Toxic Epidermal Necrolysis ( TEN ) is a rare and deadly disease. It is an extoliative dermatological disorder of unknown cause. A patient with TEN loses epidermis in sheet-like fashion leaving extensive areas or denuded dermis that must be treated like a larze, superficial, partial-thickness burn wound. The incidence of TEN has been reported at 1 to 1.3 per million per year. The female-male ratio is 3:2. TEN accounts for nearly 1% of drug reactions that require hospitalization. TEN has a mortality rate of 25 to 70%.
Smt. Anuradha Saha (in short Anuradha), aged about 36 years wife of Dr. Kunal Saha (complainant) became the unfortunate victim of TEN when she alongwith the complainant was in India for a holiday during April-May 1998. She and the complainant although of Indian original were settled in the United States of America. The complainant is a doctor by profession and was engaged in research on HIV / AIDS for the past fifteen years. Anuradha after acquiring her Graduation and Masters Degree was pursuing a Ph.D. programme in a university of U.S.A. She was a Child Psychologist by profession. Anuradha showed certain symptoms of rashes over her body and received treatment at the hands of Opposite Parties and some other doctors as outdoor patient uptil 10.05.1998 and she was admitted in Advanced Medicare and Research Institute Limited, Calcutta (for short, AMRI), on 11.05.1998, where she was treated by the above-named Opposite Parties and other doctors uptil 16.05.1998. As there was no improvement in her condition, she was shifted to Breach Candy Hospital, Mumbai, on 17.05.1998 by an air ambulance. She was treated in Breach Candy Hospital from 17.05.1998 evening till she breathed her last on 28.05.1998.
Our Complainant as husband of Anuradha felt that the doctors who treated Anuradha and the hospitals where she was treated were grossly negligent in her treatment and her death was occasioned due to gross negligence of the treating doctors and hospitals. Complainant, accordingly, got issued a legal notice to as many as 26 persons i.e. various doctors who treated Anuradha between end of April to the date of her death alleging negligence and deficiency in service on their part and claiming a total compensation exceeding Rs.55 crores from them. Complainant, thereafter filed the present complaint on 09.03.1999 before this Commission claiming a total compensation of Rs. Rs.77,07,45,000/- ( Seventy Seven Crores Seven Lakhs Fourty Five Thousand only). Later he also filed another complaint no. 179 of 2000 in this Commission against Breach Candy Hospital, its doctors and functionaries claiming a further compensation of Rs.25.30 crore ( though the said complaint was later on withdrawn), thereby making claim of compensation exceeding Rs.102 crores, perhaps the highest ever claimed by any complainant for medical negligence before any consumer fora established under the provisions of Consumer Protection Act, 1986 ( in short, the Act). These are some of the facts which make the present case extra ordinary.
The present complaint was filed by the complainant against the above-named opposite parties, namely, Dr. Sukumar Mukherjee, Dr. B. Haldar (Baidyanath Halder), Advanced Medicare and Research Institute Limited ( in short the AMRI Hospital ) and Dr. Balram Prasad and Dr.Abani Roy Chowdhury (physician) and Dr. Kaushik Nandy (plastic surgeon), the Directors of the AMRI Hospital and others claiming a total compensation of Rs. Rs.77,07,45,000/- under different heads alleging various acts of commission and omission on the part of the doctors and hospital amounting to negligence and deficiency in service. Complainant through his brother-in-law Malay Kumar Ganguly also filed criminal complaint against some of the doctors and the hospital under section 304A IPC.
The complaint was resisted by the doctors and the hospital on a variety of grounds thereby denying any medical negligence or deficiency in service on their part. Parties led voluminous documentary and oral evidence and testimonies of some of the witness were even recorded through video conferencing through a Local Commissioner. After a protracted trial and hearing and on consideration of the evidence and material so produced on record and taking note of the legal position governing the question of medical negligence, this Commission ( by a three Member Bench presided over by the then President) dismissed the complaint by an order dated 01.06.2006 holding as under:
In the result, we reiterate that Doctors or Surgeons do not undertake that they will positively cure a patient. There may be occasions beyond the control of the medical practitioner to cure the patients. From the record, it would be difficult to arrive at the conclusion that the injection Depo-Medrol prescribed by Dr. Mukherjee was of such excessive dose that it would amount to deficiency in service by him which was his clinical assessment.
Thereafter, with regard to the alleged deficiency in the treatment given to Mrs. Anuradha by Opposite Party Doctors 2, 3, 5 and 6, there is no substance. The contention against the hospital that it was not having Burns-Ward, and therefore, the deceased suffered is also without substance. Hence, this complaint is dismissed. There shall be no order as to costs.
Aggrieved by the dismissal of his complaint, the complainant filed Civil Appeal (No.1727 of 2007) in the Honble Supreme Court. It would appear that even before the said appeal was filed before the Hon'ble Supreme Court, the Supreme Court was seized of the matter in Criminal Appeal Nos.1191-94 of 2005 filed by Malay Kumar Ganguly, the complainant in the criminal complaint, against the Orders passed by the Calcutta High Court. Since the Criminal Appeals and the Civil Appeal filed by the complainant in the present complaint raised the same questions of fact and law, the Hon'ble Supreme Court heard all the appeals together and decided the same by means of a detailed judgment dated 07.8.2009. By the said order, the Apex Court dismissed the Criminal Appeals filed by Shri Malay Kumar Ganguly but allowed the Civil Appeal No. 1727 of 2007 filed by the complainant and set aside the order dated 01.6.2006 passed by this Commission dismissing the complaint and remanded the matter to this Commission for the limited purpose of determining the adequate compensation, which the complainant is entitled to receive from the subsisting opposite parties by observing as under:
So far as the judgment of the Commission is concerned, it was clearly wrong in opining that there was no negligence on the part of the Hospital or the doctors. We, are, however, of the opinion, keeping in view the fact that Dr.KaushikNandy has done whatever was possible to be done and his line of treatment meets with the treatment protocol of one of the experts viz.. Prof. Jean Claude Roujeau although there may be otherwise difference of opinion, that he cannot be held to be guilty of negligence.
We remit the case back to the Commission only for the purpose of determination of the quantum of compensation. We, keeping in view the stand taken and conduct of AMRI and Dr. Mukherjee, direct that costs of Rs.5,00,000 and Rs.1,00,000 would be payable by AMRI and Dr. Mukherjee respectively.
We further direct that if any foreign experts are to be examined it shall be done only through video conferencing and at the cost of the respondents.
Summary In view of the foregoing discussion, we conclude as under:
"The facts of this case viz., residence of the complainant and Anuradha (deceased) in USA and they working for gain in that country; Anuradha having been a victim of a rare and deadly disease Toxic Epidermal Necrolysis (TEN) when she was in India during April-May 1998 and could not be cured of the said disease despite her treatment at two superspeciality medical centres of Kolkata and Mumbai and the huge claim of compensation exceeding Rs.77 crores made by the complainant for the medical negligence in the treatment of Anuradha makes the present case somewhat extraordinary.
The findings given and observations made by the Supreme Court in its judgment dated 07.08.2009 are absolutely binding on this Commission not only as ratio decidendi but also as obiter dicta also, the judgment having been rendered by the Supreme Court in appeal against the earlier order passed by a three Member Bench of this Commission and, therefore, no attempt can be allowed to read down / dilute the findings and observations made by the Supreme Court because the Supreme Court has remitted the complaint to this Commission only for the purpose of determination of the quantum of compensation after recording the finding of medical negligence against the opposite parties and others.
The task entrusted to the Commission may appear to be simple but the facts of the present case and the voluminous evidence led on behalf of the complainant has made it somewhat arduous. Still difficult was the task of apprortionment of the liability to pay the awarded amount by the different opposite parties and perhaps it was for this reason that the Supreme Court has remitted the matter to this Commission. "
"Multiplier method provided under the Motor Vehicles Act for calculating the compensation is the only proper and scientific method for determination of compensation even in the cases where death of the patient has been occasioned due to medical negligence / deficiency in service in the treatment of the patient, as there is no difference in legal theory between a patient dying through medical negligence and the victim dying in industrial or motor accident. The award of lumpsum compensation in cases of medical negligence has a great element of arbitrariness and subjectivity. "
The foreign residence of the complainant or the patient and the income of the deceased patient in a foreign country are relevant factors but the compensation awarded by Indian Fora cannot be at par which are ordinarily granted by foreign courts in such cases. Socio economic conditions prevalent in this country and that of the opposite parties / defendants are relevant and must be taken into consideration so as to modulate the relief. A complainant cannot be allowed to get undue enrichment by making a fortune out of a misfortune. The theoretical opinion / assessment made by a Foreign Expert as to the future income of a person and situation prevalent in that country cannot form a sound basis for determination of future income of such person and the Commission has to work out the income of the deceased having regard to her last income and future prospects in terms of the criteria laid down by the Supreme Court.
There exists no straight jacket formula for apportionment of the awarded compensation amongst various doctors and hospitals when there are so many actors who are responsible for negligence and the apportionment has to be made by evolving a criteria / formula which is just going by the nature and extent of medical negligence and deficiency in service established on the part of different doctors and hospitals.
On a consideration of the entirety of the facts and circumstances, evidence and material brought on record, we hold that overall compensation on account of pecuniary and non pecuniary damages works out to Rs.1,72,87,500/- in the present case, out of which we must deduct 10% amount on account of the contributory negligence / interference of the complainant in the treatment of Anuradha. That will make the net payable amount of compensation to Rs.1,55,58,750/- (rounded ofto Rs.1,55,60,000/-). From this amount, we must further deduct a sum of Rs.25,93,000/- which was payable by Dr. Abani Roy Chowdhury (deceased) or his Legal Representative as the complainant has forgone the claim against them.
In view of the peculiar facts and circumstances of the case and as a special case, we have awarded a sum of Rs. 5,00,000/- as cost of litigation in the present proceedings.
The above amount shall be paid by opposite parties no.1 to 4 to the complainant in the following manner:
Dr. Sukumar Mukherjee-opposite party no.1 shall pay a sum of Rs.40,40,000/- (Rupees Forty Lakh Forty Thousand only) i.e. [Rs.38,90,000/- towards compensation and Rs.1,50,000/- as cost of litigation].
Dr. B. Haldar (Baidyanth Halder)-opposite party no.2 shall pay a sum of Rs.26,93,000/- (Rupees Twenty Six Lakh Ninety Three Thousand only) i.e. [Rs.25,93,000/- towards compensation and Rs.1,00,000/- as cost of litigation] AMRI hospital-opposite party no.3 shall pay a sum of Rs.40,40,000/- (Rupees Forty Lakh Forty Thousand only ) i.e. [Rs.38,90,000/- towards compensation and Rs.1,50,000/- as cost of litigation .
(iv) Dr. Balram Prasad-opposite party no.4 shall pay a sum of Rs.26,93,000/- (Rupees Twenty Six Lakh Ninety Three Thousand only) i.e. [Rs.25,93,000/- towards compensation and Rs.1,00,000/- as cost of litigation] The opposite parties are directed to pay the aforesaid amounts to the complainant within a period of eight weeks from the date of this order, failing which the amount shall carry interest @ 12% p.a. w.e.f. the date of default. "
Now again after going all through the articles and oath taken by the doctor and also the various case laws, we came to the facts of present case once again. The opposite parties have stated that the patient Late Smt Urmila Asthana had approached the opposite party no 1 on 17.06.2017 at about 12.21 AM with left side hemiparesis with right angle deviation of mouth with slight slurring of speech. The only facility available with the opposite party was Intravenous Thrombolysis . Regarding the treatment the opposite party has stated that the patient was not considered for intravenous Thrombolysis because symptoms appear in the patient while she was sleeping. When no medical treatment could be given by the opposite party, why did they not refer the patient to SGPGI ? The opposite parties knew very well that this intravenous thrombolysis should be done within three golden hours and in spite of that they did neither considered the patient fit for intravenous thrombolysis nor they advised her relatives for taking her to SGPGI .So the golden period of three hours has been wasted by the opposite parties. The opposite parties have admitted that thrombolysis is beneficial in treating stroke but it is not a sure shot treatment, as there was significant 12% increased in number of patient with minimal disability does thrombolysis would have caused more harm in the patient. If it was so, why did the opposite party not inform the wards of the patient.
MRI of the brain was done on 17.06.2014 but the time has not been mentioned there in. We are unable to stand that when the opposite party was not competent to handle the case of the patient, what was the reason to continue with her in the hospital ? Now in the present period there is facility of videoconferencing with the renowned doctors of the world regarding the treatment of any medical condition. It should have been adopted by the opposite parties but there is no evidence of it. It is also argued that at the time of admission the platelet count was 65,000 and platelet could not be given in such a condition. But all these facts had not been communicated to the family members of the patient. It was the duty of the doctor that he should inform the family of the patient about the diagnosis, about the condition of the patient and if he has no ability to treat the patient due to lack of paraphernalia, then it was on the family members to take her to some other hospital having proper facilities. When the family members of the patient knew the fact that here the life of the patient can notbe saved, thenthey took her to some other hospital where she breathed her last. Negligence in shown by the opposite party no 1 by not disclosing all the facts to the family members of the patient and they continue to treat the patient in spite of the fact that they had no best facility in their hospital and the only facility available in the hospital, that is intravenous thrombolysis and that too cannot be done on the patient, then what was the cause to continue with the patient in their hospital ? The circumstances speak themselves. These circumstances show that the opposite party has concealed the fact that they had no proper facilities for the treatment of patient and the only facility that was available with them, cannot be performed due to some reasons and in spite of all these and knowing that the patient could not survive, they did not discharge the patient but continued with the treatment, giving medicines, performing various pathological tests which was of no avail. If they could not operate the patient or could not treat the patient, keeping the patient in the hospital for making money was not proper.
We have seen in the above-mentioned articles and different case laws and also the principal of res ipsa loquitur, it is clear that the opposite parties knowingly that they could not treat the patient properly or the patient could not be revived, still they continued with the treatment mentioning different kinds of medicines and tests for which the complainant had to pay. This was not according to the noble profession of Dr we have seen in the documents. A large number of documents have been filed but we are unable to understand that when the facility of proper treatment was not in the hospital, why all these tests were done? When the opposite party knew that by thrombolysis the success rate is 10% so it should have been told to the family members of the patient and if they give their consent, the consent form should have been filled and the operation be done accordingly. But the opposite parties did not tell the family members of the patient regarding this process and its success rate, how could the family members know this fact. So it also contribute towards deficiency of service by the opposite parties.
The opposite parties have said that they have purchased insurance policies for the period by which The New India Assurance Co and the Oriental insurance Co have agreed to indemnify the opposite parties no 1 & 2 as such for any liability which may arise from the service of the hospital and the concerned Dr . If it is so they can claim insurance from the concerned insurance company.
So from the admissions of the opposite parties in their written statement and from all the facts and circumstances of the case it is a clear case of deficiency in services as knowingly the opposite parties did not refer the patient to SGPGI and kept her in their hospital tendering a bill of ₹ 227,226/- the complainant has demanded ₹ 8,747,026/as total compensation regarding transportation, Funeral expenses,et cetera. Hon'ble Supreme Court in the case of Malay Ganguly( supra) has held ;
"Multiplier method provided under the Motor Vehicles Act for calculating the compensation is the only proper and scientific method for determination of compensation even in the cases where death of the patient has been occasioned due to medical negligence / deficiency in service in the treatment of the patient, as there is no difference in legal theory between a patient dying through medical negligence and the victim dying in industrial or motor accident. The award of lumpsum compensation in cases of medical negligence has a great element of arbitrariness and subjectivity."
As argued by the opposite parties that there's no expert opinion in this case and the opposite parties cannot be held liable. Regarding the relationship of master and servant, regarding expert opinion the following judgement of Hon'ble NCDRC is reading in which the Hon'ble shall commission has quoted the judgement of the Hon'ble Supreme Court. This judgement is in relation to Sahara Hospital and Dr Sandeep Agrawal .
In the case of Gyan Mishra vs Sahara India Medical Institute ... Consumer Case no 998 OF 2015 Jt on 7 November, 2019 (NCDRC
1. GYAN MISHRA Flat No. 401, 57 Kheri House, Vishnupuri Colony, Church Road, Aliganj, Lucknow U.P. - 226 024 ...........Complainant(s) Versus
1. SAHARA INDIA MEDICAL INSTITUTE LIMITED. & ANR. THROUGH ITS CHIEF MEDICAL SUPERINTENDENT, SAHARA INDIA POINT, CTS 40-44, S.V. ROAD, GOREGAON (WEST), MUMBAI - 400 104. MAHARASHTRA.
2. Dr. Sandeep Agarwal, A-1/13, Sector 'B', Near Nehru Bal VatikaAliganj, Lucknow - 226 024.
3. Dr. Muffazal Ahmed. Zainess Hospital Compound, Near Neelkanth Sweets, Viviek Khand - 2, Gomti Naga, Lucknow - 226 010.
4. Dr. Ankur Gupta. MAX SUPER SPECIALITY HOSPITAL, MUSSOORIE DIVERSION ROAD, MALSI, DEHRADUN UTTRAKHAND - 248 001. 5. . .
...........Opp.Party(s) Hon'ble NCDRC has held "Late Shri Gyan Mishra, husband of the complainant Rupa Mishra and father of the other complainants visited opposite party No.2, Dr. Sandeep Agarwal, who is a Neurologist, for the first time on 02.5.2011 in Sahara Hospital, Lucknow. The said visit was followed by subsequent visits for consultation with Dr. Sandeep Agarwal. He was admitted in Sahara Hospital in Lucknow on 24.9.2012 and was discharged from there on 25.09.2012. During his stay in the said hospital, his pathology tests were done on 24.09.2012 and his serum creatinine was found to be 3.43 as against the range of 0.7 - 1.2. No further investigations or treatment for monitoring and management of the high serum creatinine which was indication of a kidney disease was advised to him at the time of his discharge from Sahara Hospital, nor was he advised to consult a Nephrologist for the said purpose. He was again admitted to Sahara Hospital on 09.12.2013 and was seen by Dr. Sandeep Agarwal as well as by opposite party No.3 Dr. Muffazal Ahmed, who is a Nephrologist. Opposite party No.3 informed him and his family members that the complainant was suffering from end stage renal disease and required dialysis. He was discharged from the hospital on 19.12.2013. The complainant was allegedly given iron injection during his stay in the hospital though, such injection, according to the complainant is contra indicated in the case of a person suffering from a kidney disease. This is also the case of the complainant that he was prescribed iron injection on 18.3.2014 and 26.6.2014 namely Encicarb, without checking his ferritin level.
2. Another grievance of the complainant is that the medicine Metformin was advised to him, which was contra indicated in his case and his cardiovascular examination was not done in Sahara Hospital.
3. Yet another grievance of the complainant is that a medicine namely Liofen was prescribed to him which was contra indicated in his case.
4. Alleging negligence on the part of the opposite parties in his treatment, the complainant approached this Commission by way of this consumer complaint, seeking compensation for the damages to the extent of Rs.24,81,28,253/-, along with compensation for mental agony etc., quantified at Rs.4,80,00,000/-. He also sought a sum of Rs.3.8 crores for his future medical expenses.
5. The complaint has been resisted by the opposite parties. It is stated in the written version filed by the opposite parties that the complainant was a chronic alcoholic with a long standing history of Diabetes Mellitus. He was also found to have kidney disease with Urosepsis and chronic liver disease. It is also stated that 40% of the patient with type-I or type -II diabetes mellitus develops nephropathy, which is a common cause of chronic renal failure. It is admitted that the complainant was admitted in Sahara Hospital Lucknow on 24.9.2012 and was discharged from there on 25.9.2012. The discharge, according to the opposite parties was done at the request of his relatives. It is also alleged that at the time of discharge of the complainant on 25.9.2012, it was thought that the impairment of his kidney function could be due to dehydration and should be managed conservatively. It is admitted that the complainant was seen by Dr. Muffazal Ahmed and later by Dr. Ankur Gupta, who is a Gastroenterologist when he was admitted in the hospital on 09.12.2013. It is stated in the written version that the complete iron profile of the complainant was done on 10.12.2013 and he was treated with injection 'Cresp' and oral iron but he continued to remain anaemic, despite aggressive erythropoietin and oral iron. No intravenous iron was given to him during hospitalization during December, 2013. It is further stated that when he visited the OPD on 18.3.2014, he was advised to take injection Encicarb to be infused in two hours daily for two days after a detailed discussion on pros and cons of the therapy. It is further stated that when the complainant visited OPD on 25.6.2014, he informed that he had not taken Encicarb, which was prescribed to him in March, 2014. He was therefore, advised to take the injection Encicarb. It is claimed that since erythropoietin is a costly therapy, India Society of Nephrology suggests a trial of IV Iron in anaemic chronic kidney disease if TSAT (transferrin saturation) is less than 30% and Ferritin is less than 500. The saturation of the complainant at that time was 11.42% and his serum ferritin was 258.1 on 10.12.2013. It is also claimed that it was not necessary to check ferritin before prescribing each dose of IV iron.
6. It is an admitted position that the serum creatinine of the complainant was 3.43 at the time he was discharged by opposite party No.2 Dr. Sandeep Agarwal from Sahara Hospital on 25.12.2012. A perusal of the discharge summary would show that high serum creatinine was not even noted in the said discharge summary. Despite the serum creatinine level being so high, neither any monitoring or management by way of periodical investigation was advised to him, nor was he asked to consult a nephrologist. The case of the opposite parties is that they thought that the serum creatinine level might have increased due to dehydration. The discharge summary however, does not record any such assumption. Even if the opposite party / treating doctor was of the opinion that high creatinine level could be due to dehydration, the least expected from him was to note it down in the discharge summary and advise the patient to get his creatinine level checked regularly, since the said level would have come down in due course had the same been caused by dehydration. In fact, considering the high level of serum creatinine, the opposite party No.2 Dr. Sandeep Agarwal ought to have suggested consultation by a Nephrologist to confirm the cause of the increase in serum creatinine. Therefore, it would be difficult to say that the opposite party No.2 Dr. Sandeep Agarwal was negligent in the treatment of the complainant, he having not given any treatment or advise to him for the monitoring, management and treatment of the high level of serum creatinine found nor having advised him to consult a Nephrologist during the course of his treatment and at the time of his discharge on 25.9.2012. As a result of this negligence, the complainant could not get any treatment for his kidney disease for more than one year.
7. It is an admitted position that the opposite party No.3 Dr. Muffazal Ahmed advised iron injection Encicarb to the complainant on 18.3.2014. The guidelines issued by the Indian Society of Nephrology, to the extent they deal with the administration of iron to CKD patients, read as under:-
"...... the most widely used test to asses iron status are TSAT and ferritin level. A low serum ferritin less than 30 ng / ml and TSAT less than 20% is indicative of iron deficiency. However, most CKD patients with serum ferritin more than 100 ng / ml and TSAT more than 20% do respond to supplemental iron by increase in Hb concentration and decrease in ESA dose. Hence in these guidelines we recommend, as suggested by KDIGO iron administration in anaemic CKD patients with less than 30% TSAT and less than 500 ng / ml serum ferritin, after considering the potential risk of iron administration. In CKD patients with TSAT more than 30% and ferritin more than 500 ng / ml, the safety of providing additional iron has not been studied. We do not recommend routine use of iron supplementation in these situations. Mode of Iron supplementation is either oral or IV.
Iron Status Evaluation -
3.8.1 We suggest to assess iron status (TSAT and ferritin) at least every three months during ESA therapy, including the decision to start or continue iron therapy.
3.8.2 We suggest to Test iron status (TSAT and ferritin) more frequently when initiating or increasing ESA dose, when there is blood loss, when monitoring response after a course of IV iron, and in other circumstances where iron stores may become depleted."
It would thus be seen that the treating doctor should first get the TSAT and Ferritin level of the patient checked before initiating ESA therapy. Admittedly, ferritin and TSAT of the complainant were not got checked soon before 18.3.2014 when intravenous iron Encicarb was advised to him. His ferritin levels were last checked on 10.12.2013 and more than three months had already expired by the time iron injection encicarb was advised to him on 18.3.2014. In view of the guidelines issued by Indian Society of Nephrology advising the injection Encicarb on 18.3.2014, without checking TSAT and ferritin was an act of negligence on the part of the opposite party No.3 Dr. Muffazal Ahmed in the treatment of the complainant.
Admittedly, encicarb injection was again advised to the complainant on 25.6.2014. Admittedly, his TSAT and ferritin levels were not got checked before advising encicarb to him on that date. It was solely on the basis of the report dated 10.12.2013 that the injection encicarb was advised to the complainant. The case of the opposite parties is that the complainant had told opposite party No.3 Dr. Muffazal Ahmed when he visited his clinic on 25.6.2014 that he had not got encicarb administered when it was advised to him in March, 2014. Even if this is so, considering that more than six months had already elapsed form the date the saturation level and ferritin level of the complainant were checked on 10.12.2013, it was obligatory on the party of the opposite party No.3 Dr. Muffazal Ahmed to get the said levels checked before advising encicarb to him on 25.6.2014. Though, the opposite parties have claimed that it was not necessary to get the ferritin level checked before advising each dose of iron, considering the guidelines issued by the Indian Society of Nephrology. I have no hesitation in holding that the checking of the said levels was necessary before advising intervenors iron on 25.6.2014. In fact, when the Endoscopy of the complainant was done at Fortis Memorial hospital on 01.9.2014, within about two months of his taking injection encicarb, his system was found overloaded with iron.
8. It is an admitted position that the medicine Liofen was prescribed to the complainant by opposite party No.2 Dr. Sandeep Agarwal. He was advised Liofen in December, 2012 as well as in March, 2013. The Medical Literature filed by the complainant would show that most of the patients with severely impaired renal function develop toxic symptoms after initiating a baclofen regimen. Baclofen is the compound Liofen is made of. The said literature includes that administration of baclofen, regardless of the dosages, in patients with severe impaired renal function, is not appropriate. No medical literature to the contrary, advising prescription of Baclofen with severely impaired renal function has been produced by the opposite parties. Therefore, I see no reason to reject the medical literature produced by the complainant. Opposite party No.2 Dr. Sandeep Agarwal advised Liofen (Baclofen) to the complainant not only on 25.12.2012 when his serum creatinine was very high but also in March, 2013 when it had been established that he was suffering from chronic kidney disease, prescribing Liofen to the complainant, therefore, was an act of negligence on the part of opposite party No.2 Dr. Sandeep Agarwal in the treatment of the complainant. "
Further the Hon'ble NCDRC has held ;
"12. It was also submitted by the learned counsel for the opposite parties that no expert has been examined by the complainant to prove any negligence in the treatment of late Shri Gyan Mishra. In support of his contention, the learned counsel relied upon the decision of the Hon'ble Supreme Court dated 01.10.2018 in Civil Appeal No.3971 of 2011 Dr. S.K. Jhunjhunwala Vs. Mrs. Dhanwanti Kaur &Anr. Nowhere has the Hon'ble Supreme Court said in the above referred decision that even in a simple and uncomplicated case, based on admitted facts, the negligence in the treatment of a patient can be proved, without examining a medical expert. If the matter is simple and uncomplicated, the negligence can in an appropriate case, also be proved on the basis of the admitted facts and relevant medical literature written by medical experts. A reference in this regard can be made to the decision of the Hon'ble Supreme Court in V. Kishan Rao Vs. Nikhil Super Speciality Hospital &Anr. (2010) 5 SCC 513 decided on 08.3.2010, where the Hon'ble Supreme Court inter-alia held as under:
"18. In the opinion of this Court, before forming an opinion that expert evidence is necessary, the Fora under the Act must come to a conclusion that the case is complicated enough to require the opinion of an expert or that the facts of the case are such that it cannot be resolved by the members of the Fora without the assistance of expert opinion. This Court makes it clear that in these matters no mechanical approach can be followed by these Fora. Each case has to be judged on its own facts. If a decision is taken that in all cases medical negligence has to be proved on the basis of expert evidence, in that event the efficacy of remedy provided under this Act will beunnecessarily burdened and in many cases such remedy would be illusory.
34. Therefore, the general directions in para 106 in D'Souza quoted above are with great respect, inconsistent with the directions given in para 52 in Mathew which is a larger Bench decision.
38. A careful reading of the aforesaid principles laid down by this Court in Indian Medical Assn. makes the following position clear -
(a) There may be simple cases of medical negligence where expert evidence is not required.
(b) Those cases should be decided by the Fora under the said Act on the basis of the procedure which has been prescribed under the said Act.
(c) In complicated cases where expert evidence is required the parties have a right to go to the civil court.
(d) That right of the parties to go to civil court is preserved under Section 3 of the Act.
45. It is clear from the statement of objects and reasons of the Act that it is to provide a forum for speedy and simple redressal of consumer disputes. Such avowed legislative purpose cannot be either defeated or diluted by superimposing a requirement of having expert evidence in all cases of medical negligence regardless of factual requirement of the case. If that is done the efficacy of remedy under the Act will be substantially curtained and in many cases the remedy will become illusory to the common man."
13. For the reasons stated hereinabove, I hold that the opposite party No.2 Dr. Sandeep Agarwal and opposite party No.3 Dr. Muffazal Ahmed were negligent in the treatment of the complainant, who died during pendency of this complaint. Since they were working with opposite party No.1, the said opposite party is also vicariously liable for the aforesaid negligent acts of opposite parties No. 2 and 3.
14. The next question which comes up for consideration is with respect to the quantum of compensation. Though, the complainants have claimed compensation running into crores of rupees, the facts and circumstances of the case do not justify such a huge and fanciful compensation. The complainant was alive when this complaint was instituted and he died during pendency of this complaint. There is no evidence to prove that the complainant died on account of the deficiency attributed to the opposite parties in his treatment. His creatinine level was pretty high even at the time it was checked in Sahara Hospital on 24.12.2012, though he remained untreated for the kidney disease till the same was detected by opposite party No.3 Dr. Muffazal Ahmed. In December, 2013, it is not known how much more damage to his kidney occurred during the intervening period, though it can hardly be disputed that his kidneys must have suffered further damage on account of his creatinine level having not been managed for more than one year. This is also an admitted position that after his dialysis he was discharged on 19.12.2013. Though, Encicarb was advised to him without checking his ferritin level soon before the said injection was prescribed, there is no evidence to prove the actual ferritin level of the deceased at the time the said injection was advised to him. Though, the medicine Liofen which is contrary indicated in the case of a person suffering from kidney disease was also advised to him, it is not known what damage his system had suffered on account of the consumption of the said medicine by him.
15. Considering all the facts and circumstances of the case, opposite party No.2 Dr. Sandeep Agarwal is directed to pay a sum of Rs.20.00 lacs as compensation to the complainant, whereas opposite party No.3 Dr. Muffazal Ahmed is directed to pay a sum of Rs.10.00 lacs as compensation to him. Opposite party No.1 shall be vicariously liable to pay the aforesaid amounts to the complainant. In other words, the complainant shall be entitled to an aggregate sum of Rs.30.00 lacs as compensation, out of which Rs.20.00 lacs will be payable by opposite party No.2 Dr. Sandeep Agarwal and Rs.10.00 lacs will be payable by opposite party No.3 Dr. Muffazal Ahmed. The complainant shall be entitled to recover the whole of the said amount from opposite party No.1. The opposite parties shall also pay a sum of Rs.25,000/- as the cost of litigation to the complainants.
The compensation in terms of this order shall be paid within three months form today; failing which it shall carry interest @ 9% per annum with effect from three months form the date of this order, till the date of payment."
A contraindication may be described as follows A contraindication is a specific situation in which a drug, procedure, or surgery should not be used because it may be harmful to the person.
There are two types of contraindications:
Relative contraindication means that caution should be used when two drugs or procedures are used together. (It is acceptable to do so if the benefits outweigh the risk.) Absolute contraindication means that event or substance could cause a life-threatening situation. A procedure or medicine that falls under this category must be avoided.
Some treatments may cause unwanted or dangerous reactions in people with allergies, high blood pressure, or pregnancy. For example, isotretinoin, a drug used to treat acne, is absolutely contraindicated in pregnancy due to the risk of birth defects. Certain decongestants are contraindicated in people with high blood pressure and should be avoided.
Many medicines should not be used together by the same person. For instance, a person who takes warfarin to thin the blood should not take aspirin, which is also a blood thinner. This is an example of a relative contraindication. It is not clear as to which type of contraindication was prevailing here . It was the duty of the concerned Dr to describe it in clear words to the attendant of the patient so that he could think about other alternative for the patient.
Now it is also clear that opposite party number two is the employee of opposite party number one which is the master. So it was the duty of the opposite party number one and its management committee or director or any person responsible for the administration of the hospital to inform the family members of the patient about the condition and treatment and also the treatment which was necessary but not available with the hospital but they did not do so. The doctor cannot be held liable independently because there was relationship of master and servant between opposite party no 1 & 2 . So keeping in view the above observation of the Supreme Court and the compensation awarded by the Hon'ble Supreme Court in the said case we come to the following conclusion.
The opposite party no 1 is liable to pay ₹ 4,770,000/- regarding loss of prospective future earnings of the deceased, ₹ 227,026/- towards the treatment at opposite party no 1 and Ford Hospital , ₹ 50,000/ towards funeral expenses, ₹ 1 lakh towards transportation expenses and other miscellaneous expenses due to hospitalisation, ₹ 50,000 / towards loss of income due to missed work, ₹ 35 lakhs towards loss of mother's companionship, emotional distress pain and sufferings, cost of the suit et cetera , total Rs 86,97,026/-within eight weeks from the date of judgement of this complaint case with interest at a rate of 10% from17.06.2017 and if not paid within eight weeks from the date of judgement of this complaint case the rate of interest shall be 15% per annumfrom17.06.2017 in the date of actual payment.
the complaint is allowed with costs.The opposite party no 1 is directed to pay ₹ 4,770,000/- regarding loss of prospective future earnings of the deceased, ₹ 227,026/- towards the treatment at opposite party no 1 and Ford Hospital , ₹ 50,000/ towards funeral expenses, ₹ 1 lakh towards transportation expenses and other miscellaneous expenses due to hospitalisation, ₹ 50,000 / towards loss of income due to missed work, ₹ 35 lakhs towards loss of mother's companionship, emotional distress pain and sufferings, cost of the suit et cetera , total Rs 86,97,026/-within eight weeks from the date of judgement of this complaint case with interest at a rate of 10% from17.06.2017 and if it is not paid within eight weeks from the date of judgement of this complaint case the rate of interest shall be 15% per annum from17.06.2017 till the date of actual payment.
The opposite party may reimburse this amount from the insurance company as per insurance act and rules and regulation mentioned therein after depositing/paying the amount with this court.
If the amount is not paid within the stipulated period, the complainant shall be free to file execution case at the cost of the opposite party no 1.
The stenographer is requested to upload this order on the Website of this Commission today itself.
Certified copy of this judgment be provided to the parties as per rules.
(Vikas Saxena) (Rajendra Singh) Member Presiding Member Judgment dated/typed signed by us and pronounced in the open court. Consign to RecordRoom . (Vikas Saxena ) (Rajendra Singh) Member Presiding Member Dated August 30 , 2022 JafRi, PA II Court 2 [HON'BLE MR. Rajendra Singh] PRESIDING MEMBER [HON'BLE MR. Vikas Saxena] JUDICIAL MEMBER