National Consumer Disputes Redressal
Kethiri Sai Reddy vs Apollo Hospitals on 27 April, 2010
This appeal challenges the order dated 15
NATIONAL CONSUMER
DISPUTES REDRESSAL COMMISSION
NEW
DELHI
FIRST APPEAL No. 11 of 2004
(From the Order dated 13.10.2003 in CD no. 110 of 1998 of the Andhra Pradesh
State Consumer Disputes Redressal Commission, Hyderabad)
Kethiri Sai
Reddy
7-1-212/A/40 Plot
no. 55
Shivabagh
Colony, Ameerpet
Hyderabad
Present Address-
Appellant
Flat No. 303,
Sai Aashraya Residency
Beside Nagarjuna
Nagar, Tarnaka
Secunderabad
500 017
versus
1. Apollo
Hospitals
Jubilee Hills
Hyderabad 500
033
Represented by
its Managing Director
Respondents
2. Dr. Srikant
Jawalkar
Neuro Physician
Apollo Hospitals
Hyderabad 500
033
BEFORE:
Honble Mr Justice R. C. Jain Presiding Member
Honble Mr Anupam Dasgupta Member
For the
Appellant Mr. V.
Gourisankara Rao, Advocate
For the
Respondents Mr. P.S. Narasimha, Senior Advocate
With Mrs. K. Radha Rao, Advocate
Dated 27th April 2010
ORDER
Anupam Dasgupta Aggrieved by the order dated 13.10.2003 of the Andhra Pradesh State Consumer Disputes Redressal Commission, Hyderabad (hereafter, the State Commission) in complaint case no. 110 of 1998 filed by him, the original complainant (hereafter, the complainant) has come up in this appeal.
2 (i) Before the State Commission, the complainant alleged medical negligence/deficiency in service on the part of the Apollo Hospitals, Hyderabad (opposite party, OP 1 and respondent 1 in this appeal) and the attending neuro physician at OP 1, Dr. Srikant Jawalkar (OP 2) in (initially) misdiagnosing his disease as Guillain Barre Syndrome (GBS), instead of significant compression of the spinal cord by the C5-C6 vertebra, i.e., cervical spondylosis myelopathy (CSM) from which he was actually suffering and consequently (i) causing him physical pain and mental tension for five months from mid-December 1997 to mid-May 1998, apart from infructuous expenditure on treatment of the misdiagnosed GBS and (ii) delaying the surgery that he had to undergo for his CSM, as a result of which his post-surgery recovery was adversely affected. He also alleged deficiency in service on the part of OP 1 because he was scheduled for surgery on 18.05 1998 without checking his blood sugar level (which was too high for surgery) and despite that he was sent to the operation theatre from where he had to be sent back. He further alleged that, as an in-patient, he was provided a room in which the air conditioner (a/c) did not function though he had paid for a room with a/c and this caused him bed sores, recovery from which took several weeks. For these deficiencies in service by the OPs, he claimed compensation of Rs. 18 lakh and costs.
(ii) After considering the pleadings, medical records, evidence of two doctors produced by the complainant as independent experts and the medical literature produced by the aprties, the State Commission found that there was no medical negligence on the part of the OPs. However, it partly allowed the complaint holding the OPs deficient in service in providing a room without appropriate air-conditioning facility despite charging the complainant therefore and awarded compensation of Rs. 30,000/- on that count with interest @ 12% per annum from the date of the complaint till actual payment.
(iii) The complainants appeal is thus against the State Commissions finding on the alleged medical negligence and his prayer is for enhancement of the compensation. The OPs have, however, not appealed against the order of the State Commission.
3. We have heard Mr. V. Gourisankara Rao, learned counsel for the complainant and Mr. P. S. Narasimha, learned Senior Advocate for the OPs.
Arguments of Counsel for the Parties 4 (i) On the basis of the medical record and evidence of OP 1 Hospital as well as that of the two expert doctors, Mr. Rao has argued that after the complainants admission to OP 1 Hospital in the early hours of 13.12.1997, OP 2 did not pay any heed to the cervical spine x-ray of the complainant taken on 13.12.1997 and hastily diagnosed him with GBS without first ruling out CSM. Even while the treatment prescribed by OP 1 for GBS was in progress during the in-patient stay of the complainant from 13.12.1997 to 10.01.1998 at the OP 1 Hospital, he complained repeatedly of neck/shoulder pain. However, no attention was paid to this by OP 2. Instead, after the 5-day course of a highly expensive injection of Sandoglobulin, physiotherapy was advised which further aggravated the complainants condition of CSM. The complainants neck/shoulder pain continued during the period after his first discharge from OP 1 in January, 1998 which he brought to the notice of OP 2 during his subsequent consultations as an outdoor patient at OP 1. After his second in-patient treatment at OP 1 Hospital during 27-30.03.1998 on the advice of OP 2, the complainant again went back to OP 2 with the complaint of continuing severe neck/shoulder pain on 08.04.1998 and then on 12.05.1998. It was only on 12.05.1998 that OP 2 advised the complainant to undergo an MRI of cervical spine. The MRI report dated 14.05.1998 clearly showed significant compression of the spinal cord at the C5-6 vertebra location. Thereafter, OP 2 referred the complainant to neuro surgeons at OP 1 who, after getting another neck x-ray done, advised immediate surgery. Even these surgeons planned the surgery for 18.05.1998 without noticing that the complainants serum sugar level was too high to permit any surgery, so much so that the surgery planned for 18.05.1998 had to be aborted after administration of anaesthesia. The surgery was finally conducted on 21.05.1998.
(ii) Mr. Rao further contended that the opinions of the two independent expert Doctors, namely, Dr. Suman Chandran, Professor, Department of Radiology, Osmania Medical College/Osmania General Hospital and Dr. M.R.C. Naidu, Professor and Head, Department of Neurology, Osmania General Hospital would confirm that the very first x-ray of the complainant taken on 13.12.1997 showed spondylotic changes in his cervical spine including new bone formation and this condition called for further investigation and treatment at the earliest. These expert opinions conclusively proved that OP 2 ignored both the neck x-ray of the complainant and his repeated complaints of neck/shoulder pain during the first phase of his treatment at OP 1 Hospital.
(iii) In support of his contentions, Mr. Rao also submitted voluminous medical literature on both CSM and GBS.
5 (i) On the other hand Mr. Narasimha, learned senior counsel on behalf of the OPs argued that the medical record of the complainants treatment at the OP 1 Hospital was ample proof that when the complainant approached the OP 1 Hospital on 13.12.1997, he was suffering from GBS. The diagnosis of GBS by OP 2 was entirely correct, considering the symptoms that the complainant presented as well as the results of various diagnostic tests conducted on the complainant immediately after his admission. He drew our attention specifically to the recorded symptoms, viz., absence of fever, flaccid weakness of all limbs, hyporeflexia of tendons and the results of the nerve conduction velocity tests. As noted by the State Commission in its impugned order (vide the table at internal page 7 of that order), the principal clinical features of GBS (and not of CSM) were present in the case of complainant at the time of his first admission. Further, the correctness of the diagnosis of GBS was proved by the fact that the complainants condition improved considerably after treatment for GBS, particularly because he regained the muscle power and tone of both upper and lower limbs by the time of his discharge on 10.01.1998 and was able to walk with support. It was only on 12.05.1998 that the complainant approached OP 2 for the first time with complaints of severe neck and shoulder pain and loss of control over urination. This was borne out by the complainants admission during his cross-examination before the State Commission. Simultaneous presence of severe neck/shoulder pain and incontinence being strongly indicative of CSM, OP 2 immediately advised MRI of cervical spine which showed cervical cord compression and thereafter, he referred the complainant to Dr. S.S.R. Murthy, Neurosurgeon because this condition required surgical treatment. Necessary surgery was performed as soon as the complainants condition (serum sugar level) permitted. Thus, at no stage was there any deficiency on the part of any of the treating doctors, including OP 2.
(ii) In support of his contentions, Mr. Narasimha drew attention to the extensive medical literature produced by the respondents/OPs before the State Commission as well as the compilation produced before this Commission in these proceedings. On the basis of this literature, Mr. Narasimha emphasised that both the diagnosis of GBS and its treatment by OP 2 were completely in line with the standard medical protocol in this regard.
(iii) Mr. Narasimha further emphasised that to bring home the allegation of medical negligence, the complainant was required to demonstrate conclusively that OP 2 failed the Bolam test, i.e., omitted to do something which a neuro physician of ordinary skills and competence would have done or did something that such an ordinary physician would not have done, in the course of diagnosis of the complainants ailment and his treatment thereafter. This cardinal test of medical negligence, Mr. Narasimha emphasised, had been adopted by the Apex Court as long back as in 1995 [Indian Medical Association v V.P. Shantha and Others {(1995) 6 SCC 651}] and repeatedly affirmed in all the subsequent judgements, including that in the case of Jacob Mathew v State of Punjab and Another [(2005) 6 SCC 1] and Martin F. DSouza v Mohd. Ishfaq [(2009) 3 SCC 1]. The complainant had not been able to prove that the diagnosis of GBS by OP 2 was not something that a neuro physician of ordinary skills and competence could not have made in this case. Secondly, there was no proof of the allegation that the treatment given by OP 2 to the complainant was inappropriate for his diagnosed condition, viz., GBS. Therefore, in accordance with the law laid down by the Apex Court in respect of medical negligence, the complainant had been unable to bring home his allegations, as rightly held by the State Commission.
(iv) Mr. Narasimha, however, did not contest the award of the compensation by the State Commission.
Medical Literature
6. At this stage, we may notice what some of the well-known medical websites and some standard medical textbooks have to say on GBS.
(i) Thus, the website of the National Institute of Neurological Disorders and Stroke of the Government of the USA (http://www.ninds.nih.gov/disorders/gbs/gbs.htm) states the following on GBS in simple, lay terms (because it is meant to demystify technical terms and educate the general public):
Guillain-Barr syndrome is a disorder in which the body's immune system attacks part of the peripheral nervous system. The first symptoms of this disorder include varying degrees of weakness or tingling sensations in the legs. In many instances, the weakness and abnormal sensations spread to the arms and upper body. These symptoms can increase in intensity until the muscles cannot be used at all and the patient is almost totally paralyzed. In these cases, the disorder is life-threatening and is considered a medical emergency. The patient is often put on a respirator to assist with breathing. Most patients, however, recover from even the most severe cases of Guillain-Barr syndrome, although some continue to have some degree of weakness. Guillain-Barr syndrome is rare. Usually Guillain-Barr occurs a few days or weeks after the patient has had symptoms of a respiratory or gastrointestinal viral infection. Occasionally, surgery or vaccinations will trigger the syndrome. The disorder can develop over the course of hours or days, or it may take up to 3 to 4 weeks. No one yet knows why Guillain-Barr strikes some people and not others or what sets the disease in motion. What scientists do know is that the body's immune system begins to attack the body itself, causing what is known as an autoimmune disease. Guillain-Barr is called a syndrome rather than a disease because it is not clear that a specific disease-causing agent is involved. Reflexes such as knee jerks are usually lost. Because the signals traveling along the nerve are slower, a nerve conduction velocity (NCV) test can give a doctor clues to aid the diagnosis. The cerebrospinal fluid that bathes the spinal cord and brain contains more protein than usual, so a physician may decide to perform a spinal tap. [Emphasis supplied]
(ii) One of the standard medical textbooks, Cecil Medicine (23rd Edition, Chapter 446, Peripheral Neuropathies, pp 2808-09) informs on GBS thus:
Epidemiology Acute inflammatory demyelinating polyneuropathy, the demyelinating form, is a sporadic disorder with an incidence of 0.6 to 1.9 cases per 100,000 in North America and Europe. In 60% of cases, acute inflammatory demyelinating polyneuropathy is preceded by a respiratory tract infection (e.g., cytomegalovirus, Epstein-Barre virus) or gastroenteritis (Campylobacter jejuni). Acute motor axonal neuropathy and acute motor and sensory axonal neuropathy are rare in North America and Europe but more frequent in China, Japan, Mexico, Korea and India.
Pathobiology All forms of Guillain-Barre syndrome probably result from postinfectious molecular mimicry in which nerve antigens are attacked by the immune system because they resemble antigens presented by microbes, in particular, C. jejuni. but no definitive antigen or antibody has been identified as being responsible for Guillain-Barre syndrome.
Clinical Manifestation Weakness, which is the most common initial symptom in both acute inflammatory demyelinating polyneuropathy and acute motor and sensory axonal neuropathy, can be mild, such as difficulty walking, or severe, such as a total quadriplegia and respiratory failure. Bilateral weakness of facial muscles (facial diplegia) occurs in about 50% cases. The most common manifestation is leg weakness that subsequently ascends into the arms. Although Guillain-Barre syndrome has been described as an ascending paralysis, proximal weakness is common, and 5% of cases have isolated cranial nerve involvement that subsequently descends into the limbs. Sensory loss occurs in the majority of patients. The autonomic nervous system is involved in about 65% of patients.
Diagnosis The diagnosis of inflammatory demyelinating polyneuropathy and acute motor and sensory axonal neuropathy is based on the history, physical examination, and CSF evaluation. Deep tendon reflexes are decreased or absent and the CSF is abnormal with cyclo-albuminologic dissociation. The weakness is symmetrical. The presence of CNS abnormalities should cast doubt on the diagnosis. Acute inflammatory demyelinating polyneuropathy is distinguished from acute motor and sensory axonal neuropathy by nerve conduction studies. In both acute inflammatory demyelinating polyneuropathy and acute motor and sensory axonal neuropathy, the CSF should have fewer than 5 white blood cells (WBCs/mL). If the CSF count is greater than 50 WBCs/mL, another diagnosis, such as HIV infection or Lyme disease should be considered. ..
Differential Diagnosis ..
Other entities that can mimic Guillain-Barre syndrome are acute spinal cord compression, acute transverse myelitis and vascular myelopathies, all of which are characterised by decreased reflexes before the development of upper motor neuron signs such as increased reflexes. Carcinomatous or lymphomatous meningitis can also cause a rapidly developing quadriparesis, but both are associated with elevated CSF WBC counts.
Treatment Patients with Guillain-Barre syndrome require hospitalisation because of the potential for respiratory compromise. Pulmonary function tests should be performed frequently; a vital capacity of less than 1 L or a negative inspiratory force of less than 70 suggests that ventilator support may be needed in an intensive care unit setting. Autonomic instability and difficulty swallowing also need to be monitored.
Nonspecific therapies directed at modulating the immune system are effective in Guillain-Barre syndrome. For example, plasma exchange, usually four exchanges of 1.5 L of plasma spread over a 10-day period is considered the gold standard therapy. Two plasma exchanges may be sufficient in mild cases, and six exchanges are not superior to four in severely affected patients. This therapy should ideally be administered within the first 2 weeks and nor later than 4 weeks from clinical onset.
Intravenous immunoglobulin (IVIG) therapy, given as 2 g/kg divided over 2 to 5 days within the first 2 weeks, is as effective as plasma exchange. Because plasma exchange and IVIG are equally effective, at least in the first two weeks, IVIG is often preferred for its convenience unless there are contraindications, such as low serum IgA levels, renal failure, or severe hypertension.
Ten per cent of patients with Guillain-Barre syndrome relapse after initially responding to plasma exchange or IVIG; they usually respond to a second cycle of the previously effective treatment. The combined use of plasma exchange followed by IVIG does not improve the prognosis.
Corticosteroids in different forms (intravenous methylprednisolone, oral prednisolone or prednisone, intramuscular addrenocorticotropic hormone) are not of benefit. A recent trial of intravenous methylprednisolone (500 mg/day for 5 days) in association with IVIG versus IVIG alone showed a slight initial advantage for the combined treatment but no benefit in terms of long-term disability. [Emphasis supplied all through]
(iii) Similarly, Harrisons Principles of Internal Medicine (17th Edition, Chapter 380, pp 2667-72) has the following on GBS:
Guillain-Barre syndrome (GBS) an acute, frequently severe, and fulminant polyradiculoneuropathy that is autoimmune in nature occurs year-round at a rate of about one case per million per month in the United States and Canada. ... ... ... ... ... ... ... ... ...
Clinical Manifestations GBS manifests as rapidly evolving areflexic motor paralysis with or without sensory disturbance. The usual pattern is an ascending paralysis that may be first noticed as rubbery legs. Weakness typically evolves over hours to a few days and is frequently accompanied by tingling dysesthesias in the extremities. The legs are usually more affected than the arms, and facial diparesis is present in 50% of affected individuals. The lower cranial nerves are also frequently involved, causing bulbar weakness with difficulty handling secretions and maintaining an airway; the diagnosis in these patients may initially be mistaken for brainstem ischemia. Pain in the neck, shoulder, back, or diffusely over the spine is also common in the early stages of GBS, occurring in ~50% of patients. Most patients require hospitalization, and almost 30% require ventilatory assistance at some time during the illness. Fever and constitutional symptoms are absent at the onset and, if present, cast doubt on the diagnosis. Deep tendon reflexes attenuate or disappear within the first few days of onset. Cutaneous sensory deficits (e.g., loss of pain and temperature sensation) are usually relatively mild, but functions subserved by large sensory fibers, such as deep tendon reflexes and proprioception, are more severely affected. Bladder dysfunction may occur in severe cases but is usually transient. If bladder dysfunction is a prominent feature and comes early in the course, diagnostic possibilities other than GBS should be considered, particularly spinal cord disease. Once clinical worsening stops and the patient reaches a plateau (almost always within 4 weeks of onset), further progression is unlikely.
[Note; The textbook also describes four sub-types of GBS, viz., Acute Inflammatory Demyelinating Polyneuropathy (AIDP), Acute Motor Axonal Neuropathy (AMAN), Acute Motor Sensory Axonal Neuropathy (AMSAN), and M. Fisher Syndrome (MFS) in Table 380-1. AIDP is relevant in this case, as this is what OP 2 claimed to have diagnosed the complainant with.] Antecedent Events Approximately 70% of cases of GBS occur 1-3 weeks after an acute infectious process, usually respiratory or gastrointestinal. Culture and seroepidemiologic techniques show that 20-30% of all cases occurring in North America, Europe, and Australia are preceded by infection or reinfection with Campylobacter jejuni. A similar proportion is preceded by a human herpes virus infection, often CMV or Epstein-Barr virus.
Laboratory Features CSF findings are distinctive, consisting of an elevated CSF protein level [1-10 g/L (100-1000 mg/dL) without accompanying pleocytosis. The CSF is often normal when symptoms have been present for <48 h; by the end of the first week the level of protein is usually elevated. A transient increase in the CSF white cell count (10-100/L) occurs on occasion in otherwise typical GBS; however, a sustained CSF pleocytosis suggests an alternative diagnosis (viral myelitis) or a concurrent diagnosis such as unrecognized HIV infection. Electrodiagnostic features are mild or absent in the early stages of GBS and lag behind the clinical evolution. In cases with demyelination, prolonged distal latencies, conduction velocity slowing, evidence of conduction block, and temporal dispersion of compound action potential are the usual features.
Diagnosis GBS is a descriptive entity. The diagnosis is made by recognizing the pattern of rapidly evolving paralysis with areflexia, absence of fever or other systemic symptoms, and characteristic antecedent events. Other disorders that may enter into the differential diagnosis include acute myelopathies (especially with prolonged back pain and sphincter disturbances); botulism (pupillary reactivity lost early); diphtheria (early oropharyngeal disturbances); Lyme polyradiculitis and other tick-borne paralyses; porphyria (abdominal pain, seizures, psychosis), vasculitic neuropathy (check erythrocyte sedimentation rate, described below);
poliomyelitis (fever and meningismus common); CMV polyradiculitis (in immunocompromised patients); critical illness neuropathy; neuromuscular disorders such as myasthenia gravis; poisonings with organophosphates, thallium, or arsenic; tick paralysis; paralytic shellfish poisoning; or severe hypophosphatemia (rare). Laboratory tests are helpful primarily to exclude mimics of GBS. ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ...
Treatment In the vast majority of patients with GBS, treatment should be initiated as soon after diagnosis as possible. Each day counts; ~2 weeks after the first motor symptoms, immunotherapy is no longer effective. Either high-dose intravenous immune globulin (IVIg) or plasmapheresis can be initiated, as they are equally effective. A combination of the two therapies is not significantly better than either alone. IVIg is often the initial therapy chosen because of its ease of administration and good safety record. IVIg is administered as five daily infusions for a total dose of 2 g/Kg body weight. ... ... ... ... .
In the worsening phase of GBS, most patients require monitoring in a critical care setting, with particular attention to vital capacity, heart rhythm, blood pressure, nutrition, deep vein thrombosis prophylaxis, cardiovascular status, early consideration (after 2 weeks of intubations) of tracheotomy, and chest physiotherapy. [Emphasis supplied all through]
(iv) After careful perusal of the variety of medical literature on GBS, consisting of extracts of chapters from some other medical textbooks and also articles from some websites, produced by both the parties, we are unable locate any information of significance over and above or different from that in the literature reproduced above. Hence, in determining the issues involved in this appeal we do not find it useful to reproduce the information from these references cited by the parties.
(v) As regards CSM, the parties have once again cited some printed medical literature. In this context, two independent experts who saw the x-ray and MRI plates of the complainant, were examined and cross-examined before the State Commission. In our view, their evidence would carry greater value than reference to the information of general nature in the printed medical literature on CSM so far as the specific case of the complainant is concerned.
Discussion 7(i) We have carefully considered the submissions of the learned counsel for the parties and have gone through the entire medical record as well as the evidence of the complainant, OP 2 and the two above-mentioned Doctors brought in as expert witnesses before the State Commission.
(ii) We may note that in the course of his first in-patient treatment at OP 1 during 13.12.1997 to 10.01.1998, the complainant did complain of shoulder/neck pain on several occasions. These, as noted in the medical record (including that of physiotherapy) produced by the respondents/OPs, were on 15.12.1997, 19.12.1997, 22.12.1997, 23.12.1997, 27.12.1997, 29.12.1997, 02.01.1997 and 10.01.1998. However, there is no record of any diagnostic/medical notice (except application of hot pack once and administration of analgesics) being taken of this complaint which, as averred by the complainant, persisted even after his discharge.
(iii) The main ground for diagnosing the condition of the complainant as GBS (AIDP, to be precise, according to the statement of OP 2) was that the symptoms as well as nerve conduction velocity studies logically led to this diagnosis. In fact, among the documents submitted by the respondents/OPs before the State Commission, there was a comparative chart of the clinical features of CSM vis--vis GBS seeking to emphasise this point and the comparison was relied upon by the State Commission in arriving at its finding in the impugned order. This chart sought to impress that all the five principal clinical features presented by the complainant were those of GBS and not CSM. However, in his cross-examination before the State Commission, OP 2 stated, inter alia The symptoms of cervical spondylosis and GBS can be the same. and, MRI is not necessary to confirm cervical spondylosis. Yet on 12.05.1998 (when according to him, the complainant approached him, for the first time, with the complaints of severe neck/shoulder pain and bladder incontinence), the only diagnostic test that he advised the complainant was an MRI of his cervical spine.
(iv) When asked why the findings of the complainants neck x-ray done on 13.12.1997 were not noted in his discharge summary dated 10.01.1998, OP 2 merely stated that the discharge summary being prepared by the Residents, this (lack of mention of the neck x-ray findings) would probably be due to oversight of the Residents. This discharge summary was not signed by OP 2. However, we find from the medical record that the discharge summary after the complainants surgery for CSM in May 1998 was signed by the treating neurosurgeon also.
(v) OP 2 also made the following statement in his cross-examination:
It is not true to suggest that G.B. Syndrome is a rare case. I cannot say whether it affects one in one million operations (sic persons?). I cannot give the figure as to how many cases of GBS were treated upto 1999 in Apollo Hospital. I come across two to three cases of GBS in a month on an average.
(vi) (a) Dr. Suman Chandra, Professor in Radiology deposed before the State Commission that the complainants AP view cervical spine x-ray dated 19.12.1997 showed rudimentary cervical ribs on both sides and, The rudimentary cervical ribs are abnormal means extra growth. As regards the MRI of 13.05.1998, he stated, The said MRI reveals cervical spondylosis changes with displacement of C6 vertebral body posteriorly with impression on cervical cord. Though he commented on two more x-rays of the complainant, these were objected to by the counsel for the Ops because these x-rays were not taken at the OP 1 Hospital and one of them did not have the date. There was an attempt during Dr. Chandras cross-examination to draw him out on whether cervical spondylosis was common in general population who are otherwise healthy but Dr. Chandra replied, Please ask any physician or surgeon for the answer. When questioned by the counsel for the OPs if the presence of spondylosis in x-ray always meant that the patient had neurological disease due to spondylosis, Dr. Chandra replied, The neurophysician or neurosurgeon can answer this question.
(b) Dr. M. R. C. Naidu, Professor in Neurology, however, deposed at greater length. In his examination-in-chief, he inter alia stated, Cervical spondylosis is a degenerative disease which usually comes in elderly people and can be aggravated by increased physical stress and strain. It develops over a period of few months or years and can aggravate suddenly due to trivial trauma. Trivial trauma means sudden excessive movements of neck which can precipitate the problem.
Ex. C1 shows spondylosis changes in the cervical spine which includes new bone formation. Ex. C2 also shows spondylosis changes along with anterior- posterior subluxation of C5 over C6. Subluxation means altered alignment of bones in the neck. Compression of the spinal cord in this patient based on the Ex. C2 is likely but needs further confirmation by MRI. Ex. C7 (a) and (b) confirm long-standing compression by (sic of?) spinal cord at C5/C6 level. This finding also suggests that that the recovery after surgery is unlikely to be complete. It means even after the surgery patient is likely to improve his condition but not completely. There are no grades of compression of the spinal cord. As per MRI report Ex. C7 (a) and (b) the patient requires surgery of his neck. The findings of Ex. C1 to C3 are correlating with the findings of Ex. C7
(a) and (b) (MRI).
This type of patient will have pain in the neck and also both upper limbs along with weakness of hands and legs.
For confirmation of extent of compression of the spinal cord we need to get MRI which is necessary. The earlier the operation has the chances of improvement are better (sic the earlier the operation, the better are the chances of improvement?). If this surgery is delayed the recovery will not be as good as earlier surgery (sic as that with earlier surgery?).
GB Syndrome is a non-neurosurgical condition. The neuro physician is the right person to diagnose and treat the GB Syndrome patient. The x-rays and the MRI pictures (Ex. C1 to C3 and C7 (a) and (b)) do not say anything about GB Syndrome but only show that there is cervical cord compression.
When questioned in cross-examination if it was quite common for people of more than 45 years of age to show spondylotic changes in the (cervical - supplied) x-ray, Dr. Naidu replied, Yes. It is quite common in the people of above 45 years age to (sic - show?) spondylosis changes in the x-ray.
When further cross-examined if the presence of spondylosis in x-ray always meant that the patient had neurological disease due to spondylosis, Dr. Naidu replied in the negative.
To another question during his cross-examination regarding proper investigation to diagnose GB Syndrome, Dr. Naidu stated, As far as clinical picture which is important more than any investigation (sic As far as GBS is concerned, clinical picture is more important than any investigation?). CSF findings and EMG help for diagnosing this condition. X-ray or MRI does not help in diagnosing GB syndrome.
I do not comment on the nerve conduction studies because I am not the right person. GB Syndrome can also cause weakness of hands and legs. It is possible for the coexistence of GB Syndrome and cervical spondylosis (sic It is possible for GB Syndrome and cervical spondylosis to co-exist?).
Conclusions
8. After careful consideration of the pleadings, evidence and documents on record as well as the relevant medical literature, we come to the following conclusions:
(i) It is amply clear that given the symptoms that the complainant presented himself with on 13 December 1997 and the results of the diagnostic tests performed on him, OP 2 was justified in diagnosing him with GBS. The treatment administered by OP 2 for GBS (viz., intravenous injection of immunoglobulin, including the dosage thereof) was also in accord with the standard protocol, as the medical literature cited above shows. Though neither medical textbook referred to above mentions the need for physiotherapy after administration of IVIg, the website of the National Institute Neurological Disorders and Stroke, USA mentioned above states, Often, even before recovery begins, caregivers may be instructed to manually move the patient's limbs to help keep the muscles flexible and strong. Later, as the patient begins to recover limb control, physical therapy begins. [Emphasis supplied] This would show that post-IVIg administration, physiotherapy, as given to the complainant, was necessary. Dr. Naidu, a Professor of Neurology and one of the expert witnesses brought in on behalf of the complainant, deposed unambiguously that a neuro physician (which, OP 2 was) was the right medical person to diagnose and treat this condition of GBS. Hence, the main allegation in the complaint that GBS was a mis-diagnosis or that the treatment was inappropriate is neither supported by the facts of the case nor the standard medical literature.
(ii) (a) However, it is equally clear that OP 2 completely brushed aside the possibility of the complainant also suffering from CSM and the consequences of delay in commencement of treatment for that disease. Besides the explicit caution in Cecil Medicine that some other diseases, including acute spinal cord compression, could mimic the symptoms of GBS, it needs to be noticed that OP 2 himself admitted that the symptoms of CSM and GBS could be the same (vide paragraph 7 (iii) above). Though OP 2 claimed that he had seen the cervical spine x-ray of the complainant taken on 19.12.1997, he stated that this reflected cervical spine changes common to most persons of the age group as that of the complainant. However, that reading was not what a physician of ordinary skill and prudence would have concluded, as is very clear from the deposition of both Dr. Chandra and Dr. Naidu. Dr. Chandra stated that the first x-ray showed rudimentary cervical ribs on both sides and Dr. Naidu confirmed that the said x-ray showed spondylotic changes including formation of new bone. He went ahead to add that the findings of the first x-ray (and others, including the one to which OPs objected during the examination before the State Commission) correlated with that of the MRI of May 1998. Thus, OP 2 owed a duty of ordinary care to the complainant to investigate further the complainants cervical neck condition and if he needed treatment, simultaneously, for his spondylotic cervical changes instead of claiming that these changes were merely due to his age; as such changes were common for that age group. His contention that the complainant presented himself with symptoms signifying CSM for the first time on 12.05.1998 is also belied by the medical record showing numerous complaints of shoulder/neck pain by the complainant even during the period of his first in-patient treatment at OP 1 Hospital during December 1997 January 1998; the first-time complaint in May 1998 was of lack of bladder control, which would only show that the condition had worsened during the period since December 1997. This would demonstrate that despite being the sole treating physician during this period, OP 2 did not take notice of the (repeatedly voiced as well as recorded) complaints of shoulder/neck pain of the patient while the latter was entirely in his care. This was no case of simple error of judgment.
For, it can be no treating physicians case, howsoever ordinary in skills and competence, that having once diagnosed a patient with a particular disease and treating him for that, he was not required to take medical notice of any other persistent complaint of such a patient, particularly when the said complaint reflected symptoms with a direct relevance to another medical condition that the result of at least one of the diagnostic tests (viz., cervical neck x-ray) also pointed to (viz., CSM, in this case). One may also notice the expert opinion of Dr. Naidu that GBS and CSM could co-exist in a patient.
(b) This attitude of completely ignoring the spondylotic changes in the cervical spine of the complainant, despite the x-ray of 19.12.1997 and the complainants repeated complaints of shoulder/neck pain over a long period of nearly 28 days of in-patient treatment during 1997-98 is re-affirmed by the omission of the x-ray findings from being even mentioned in the discharge summary of 10.01.1998. The plea of OP 2 that the said discharge summary was prepared by a Resident who might have overlooked the matter is further indicative of the lack of ordinary care on the part of OP 2. That it was the practice of the treating doctor at OP 1 Hospital to sign the discharge summary of a patient (in addition to the Resident preparing the said document) is borne out by the fact that the treating neuro surgeon did sign the discharge summary of the complainant after his surgery for the CSM in May 1998.
(c) As a point of general application, we are of the considered view that a treating physician must see the discharge summary himself for its accuracy and completeness and sign it because this summary not only records the history of complaints, clinical findings of examination at the beginning, diagnostic tests and their results, provisional and final diagnosis of the disease and treatment administered but also the condition of the patient at the time of his/her discharge, any special features (e.g., sensitivity to drugs), any chronic or systemic ailment of the patient (e.g., hypertension, diabetes mellitus) apart from the specific one for which he was treated as an in-patient, etc., and further advice on medication/treatment and follow-up. This summary is the only complete document that a patient leaves the hospital with. Its importance cannot be overemphasised.
(d) It is, therefore, unacceptable that the duty of care expected of a physician of ordinary skills and competence, a la Bolam (as enunciated by a three-Judge bench of the Apex Court in the Indian Medical Association case - supra) could be so loosely construed as to exempt such a physician (particularly, in an exclusive, private hospital not inundated with incessant flow of a multitude of patients like a public hospital run by the Government or a local body) from the responsibility to see what his (or, the Hospitals) Resident wrote or did not in a singularly important document like the discharge summary for a patient. Even in the case of Martin F DSouza (supra) relied upon by Mr. Narasimha, the Apex Court emphasised the need for full record of diagnosis, treatment, etc., being maintained (vide paragraph 47 (f)).
(iii) The gravity of the above-mentioned lapse on the part of the OP 2 in terms of the post-surgery prognosis of the complainant for his CSM is established by the unequivocal medical opinion of Dr. Naidu that the recovery in the case of delayed surgery for CSM would not be satisfactory. This what the complainant also alleged in his complaint.
(iv) The deposition of OP 2 before the State Commission that it was not true that GBS was a rare disease reflects another dimension of his professional knowledge (and overall attitude) that needs to be viewed with his further statement on the incidence of GBS that at the OP 1 Hospital he dealt with two to three cases in a month on an average. Apart from the description of GBS as a rare condition in the website of the National Institute Neurological Disorders and Stroke, USA (vide paragraph 6(i) above), Harrisons Internal Medicine informs (vide paragraph 6(iii) above) that cases of GBS occur at the rate of one case per million per month in the USA, Canada, etc. Cecil Medicine, on the other hand, puts down the incidence to 6 to 19 cases per million per annum or 0.5 to 1.5 per million per month. For the claim of OP 2 to be statistically valid (at the same epidemiological rate of one case per million per month in India a reasonable assumption), OP 1 Hospital would have to be treating about 2 to 3 million patients per month at the relevant time. To put it mildly, we do not find any such averment of OP 1 on record and hence this claim of OP 2 needs to be taken with, not a pinch but, several kilograms of salt. The average physician of ordinary skills and competence is surely not expected to make prima facie exaggerated claims of his experience of dealing with a particular disease/condition/syndrome with a view to asserting the correctness of his diagnosis of that disease/condition/syndrome in a particular patient. We have already noticed that the statement of OP 2 on MRI not being necessary to confirm CSM was, apart from being at complete variance with the opinion of Dr. Naidu, belied by his own conduct of advising MRI to the complainant on 13.05.1998.
(v) The complainant was admitted to OP 1 Hospital on 16.05.1998 for surgery relating to his CSM. He was fixed up for surgery on 18.05.1998. The medical records produced by the OPs do not show that the pre-operative check-up to assess his fitness for surgery included his blood sugar level. On 18.05.1998, he was wheeled into the operation theatre at 09.15 a.m. only to be sent back to his room at 11.45 a.m. because his blood sugar level was found to be excessive. Though the records produced by OP 1 do not show when and how this discovery was made on 18.05.1998, the fact remains that he was scheduled for surgery without as basic a pre-operative test as that of blood sugar. He had to be put on intensive treatment for diabetes mellitus for the next three days before he could be operated upon for his CSM on 21.05.1998. If this is not an example of less-than-ordinary medical care, we wonder what would be.
9. In view of the foregoing discussion, it has to be held that while no medical negligence can be attributed to OP 2 in respect of his diagnosis and treatment of the complainant for GBS, OP 2 was negligent in not considering, with the care expected of a physician of ordinary skills and prudence, further diagnostic tests to ascertain the cause of the complainants repeated complaints of shoulder/neck pain during his first round of in-patient treatment (13.12.1997 10.01.1998) at the OP 1 Hospital, particularly when the complainants cervical spine x-ray of 19.12.1997 clearly showed spondylotic changes. OP 2 was also negligent in not recording (or, ensuring his Resident to record) in the complainants discharge summary of 10.01.1998 the fact that he had undergone a cervical spine x-ray during the said period of treatment and that the x-ray showed spondylotic changes. Because of these acts of negligence, the complainants treatment/surgery for CSM was unduly delayed, causing him physical pain and reducing his chances of recovery even after the surgery for CSM which was ultimately carried out in May 1998. Finally, though the complainant was admitted to the Hospital for surgery for CSM on 16.05.1998, the doctors/staff at the OP 1 Hospital was negligent in not checking up his blood sugar level in the course of standard pre-operative check-ups and still sending him to the operation theatre on 18.05.1998 from where he had to be sent back in a couple of hours. Needless to add, the complainants allegation about not being provided an air conditioned room was not even contested by OP 1. For these acts of negligence, the complainant is entitled to suitable compensation.
10. Consequently, we allow the appeal partly and set aside the findings and order of the State Commission. As regards the quantum of compensation, we find that the sum claimed by the complainant is excessive. The expenditure on his treatment at the OP 1 Hospital for both GBS and CSM could not have been avoided for he suffered from both these ailments. He cannot, therefore, claim anything on these counts. For the physical pain and compromised prognosis of recovery due to the negligence which caused delay in the diagnosis and treatment of CSM, negligence in the pre-surgery investigations not including examination of the blood sugar level prior to the surgery for CSM and that in not providing a room with the type of facility paid for, a lumpsum compensation of Rs. 2 (two) lakh to the complainant, payable jointly and severally by OP 1 Hospital and OP 2 doctor would, in our view, meet the ends of justice in this case. We order accordingly and direct the OPs to pay this amount to the complainant within four weeks of the date of this order, failing which the amount shall carry interest @ 9% per annum. There shall be no order as to costs.
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[R. C. Jain, J] [Anupam Dasgupta]