NATIONAL CONSUMER DISPUTES REDRESSAL COMMISSION
1. Smt. Geetu Sapra
w/o Late Shri Rajiv Sapra
2. Master Karan Sapra (Minor) ]
s/o Late Shri Rajiv Sapra ] Through mother &
] Natural Guardian
3. Master Kunal Sapra (Minor) ] Smt.Geetu Sapra
s/o Late Shri Rajiv Sapra ]
All Residents of :
B-6/1 Mianwali Nagar
1. Dr. B.L. Kapoor Memorial Hospital
2. Dr. K.P. Mishra
C/o Dr. B.L. Kapur Memorial Hospital
Alternative Address :
GD-86 Pitam Pura
3. Dr. (Mrs.) J. Sethi
Senior Consultant (Anaesthetist)
C/o Dr. B.L. Kapur Memorial Hospital
Alternative Address :
C-4, CGHS Dispensary
Dr.Zakir Hussain Marg
Junior Consultant (Anaesthetist)
C/o Dr. B.L. Kapur Memorial Hospital
MRS. RAJYALAKSHMI RAO, MEMBER
For the Complainant : Mr.Lalit Bhasin, Advocate with Ms.Renu
Verma and Ms.Shivani Yadav,
For Opp. Party No.1 : Mr.J.R. Midha, Advocate with Mr.Neeraj
Singh and Mr.Laxmi Chand, Advocates
For Opp. Party No.3 : Mr.Rajeev Sharma, Advocate
For Opp. Party No.4 : Mr.Bhupinder Mehtani, Advocate
It is the contention of the complainant
that Rajiv Sapra was a young
man of 32 years and was a graduate in Commerce and that he was an exporter of
repute and was partner of Vikrant Exports,
The first point that requires our decision is:
.I. Whether the Complaint before the Consumer Fora is maintainable in a case where claim before the Motor Vehicles Accident Tribunal is pending?
At the outset, learned counsel appearing on behalf of the respondents submitted that for the accidental death the complainant has filed a claim petition before the Motor Accident Claims Tribunal [MACT for brief] which is still pending. Therefore, the present complaint, before the Consumer Forum for the same cause, is not maintainable .
Against this, the learned counsel, Mr.Bhasin, submitted that this question was previously
agitated by the respondent and that contention was accepted by this
Commission. Hence, the complainant was required to file Civil Appeal No.2/2003
Hence, the cause of action for filing Claim Petition before the MACT is the accident arising out of the negligence of the driver of the other vehicle. As against this, before the Consumer Fora, the complaint is maintainable on the ground that there was deficiency in service by the hospital and/or the doctors while giving treatment to the deceased. Such complaint/claim cannot be filed before the MACT as MACT would not have the jurisdiction to decide whether there was deficiency in service by the doctors or the hospital.
Hence, the submission of the Complainant requires to be accepted, because the two causes are different and are required to be decided by separate Tribunals/Forums having limited jurisdictions.
(a) the cause of action before the MACT was, with regard to rash and negligent driving by the Driver of the other vehicle by which accident was caused; and
(b) the cause of action against the Doctors or the hospital is for deficiency in rendering service or treatment by the hospital and the doctors.
Both causes are separate and distinct.
Further, in the present case, the accident resulted in death. Therefore, the complaint before MACT is maintainable. Before the Consumer Fora it is maintainable as it is alleged that there was deficiency in service by the hospital in not giving proper treatment at appropriate time. It is to be made clear that in case of accident, even if proper treatment is given, patient may or may not survive. In the present complaint, we are concerned only with deficiency in rendering proper treatment to the deceased Mr.Sapra, who might or might not have survived despite proper treatment. The claim is to be limited only with regard to the deficiency in service in not giving proper treatment at proper time. Hence, the complaint for such deficiency in service is maintainable.
II. Deficiency in service by the Hospital & Doctors;
The next question would be with regard to the deficiency in service by the respondent hospital and the doctors. For this purpose, we would first refer to the case summary given by Respondent No.1. The relevant part thereof is as under:
A case of fracture of shaft femur right named Mr. Rajiv Sapra 32 years (M) resident of H. No. B6 1A, Main wall, Rohtak Road, New Delhi) admitted in this Hospital on 2.11.1992 at 12.30 P.M. Patient was giving history of Road side accident on 1.11.1992, this is history of unconsciousness at the time of accident for short time.
At the time of admission patient was conscious, pulse 100 per minute regular, a febrile, pupils were normal. Swelling over right thigh to tenderness ++. Patient was admitted under the treatment of Dr. Mishra.
Dr. Mishra examined the case on 2.11.1992 and decided for open reduction and internal fixation. Preanaeothetist check up done on 2.11.1992 evening by Dr. S.P.Singh, Anaesthetist and found to be fit for anesthesia.
On 3.11.1992 case was taken in the operation theater for open reduction at 11.30 A.M. Anaesthetist ( Dr. Sethi, Senior Consultant, Dr. Lamba, junior Consultant ).
Pulse 84 per minute BP 120/80 min/Hg. Intra venous (i/v) line started C- R/L then spinal anaesthetia given by 2.5. ml. of sensorcors. Patient was stable but little apprehensive so injection fortwin 15 mg. and injection Phonegan 125 intra venous (i/v) given. Intra venous (i/v) fluid in 01.R/L 10 and DNS 28 i/v given. Around patient was moving his legs so injection ketain 50 mg + injection atrophine 0.6 mg. i/v. After about 15 minutes at the end of surgery a blue leg was noticed by anaesthetist. Patient became restless sweating and techycardia. Pulse become imperceptible.
Immediately all resuscitative measures taken. Orotrachel intubation done. Positive Pressure Ventilation (PPV) 180/02 then injection Atropine 0.6 injection sodabicarb 100 mg. Injection Elforcin 200mg Injection Maphetine 15mg. i/v. given. Pulse 64 per minute again injection Atropine 0.6 mg. given. Remaining skin closure completed. BP was 86 systolic. Then injection Msphentime 15mg given and Dopamine drip (2 AMP 5% Dex) started physician called. Chest was full of crepts so injection Lasix 40mg. Intra venous given.
Dr. Bedi (physician) attended the case, then x-ray chest Apview and ECG Blood sugar urine exam done. X-ray chest was showing Pulmonary Oedema ECG showing Sinus techycardia with HR 160 per minute. No St and T chagres urine sugar +++. Urine ketone bodies Negative.
Again case seen by Dr. Jaswant Singh ( Senior Physician ) Injection Lasix. 40mg. + 60 mg. injection Deriphylline intra venous given IPPV constant. Patient shifted to ICU. In the ICU Manitol 350 ml. Intra venous given. Injection Omnatex I G stat. and injection soluble insulin 10 unit stat. At Resp 30 per minute BP 110/40 injection Decadron 32 mg. I/V stat given. Blood for NA, K.CI. HCO3, CPI, CPKMB sent.
Patient continued on PPV wiht 100% o2. At case seen by Dr. Jaswant Singh
Physician and Dr.K.K.Malhotra (Senior Physician,
Blood gas analysis done, Cyanosis persisted then it is decided ( by Senior Anaesthetis and Senior
Physician) that patient to be put on Respirator. But hospital respirator was found not to be
functioning satisfactorily. Various hospitals were contacted for bed with
respirator facilities but Bed available at
From this case summary, it is apparent that
i) on 2.11.1992 nothing unusual was noticed by the doctors of Respondent No.1 hospital;
ii) On 3rd at about at the end of surgery, a blue leg was noticed by Anaesthetist, patient became restless sweating and techycardia, pulse become imperceptible;
iii) X-ray was taken which was showing Pulmonary Oedema;
iv) ECG was showing Sinus Tachycardia;
v) The hospital respirator was found not to be functioning satisfactorily;
Various hospitals were contacted for bed with
respirator facilities and the bed was available at
there is a case summary by
On admission he was in a deeply comatose state. On examination the PR was 160 pmt, regular, BP 90.40 (RA supine),. Temp.103 F cold and clammy to touch with central and peripheral cyanosis. He was not responding to even the deepest painful stimuli and no reflexes were elicitable including the planters. The pupils were near normal in size but not reacting to light and the fundus revealed hazy but normal discs. The patient was brought with endotracheal tube in site and examination of the chest revealed bilateral coarse coarse crepts scattered all over the chest with very rapid and shallow breathing. The heart sounds were normal ( SUBS2N) and no additional sounds were heard. The abdomen was soft with minimal bowel sounds and urinary catheter in situ. The right leg was encased in a P.O.P east with drain in situ: There was also a deep infected cash on the right forearm.
The general condition gradually improved and from and on 07.11.92 the PR was normal, BP was maintained without vasopressors and adequate fluid and electrolyte balance maintained. Ventilation with 40% oxygen was continued and the acid base balance and blood cases were in the acceptable range. The urinary output was also maintained well. On neurological examination the pt. had positive eyelash reflexes conjuctival reflex, reflexes, movement of the limbs on painful stiluli, carnal reflex, deglutition reflex, and corneal reflex with brisk deep fondus reflexes.
However, pupillary reflex was singularly absent.
In conclusion our opinion is that patient suffered from prolonged hypoxia, Hypercarbia and Hyperacidosis leading to all irreversible tissue damage including Brain and ultimately died in spite of intensive therapy.
From the aforesaid case summary, we have to find out whether there is deficiency in service by Respondent No.1 hospital or Respondent No.2 Dr.K.P. Mishra. Further there is nothing against Respondents No.3 and 4.
As quoted above, the conclusion arrived at by the Doctors of the Ashlok Hospital clearly establishes that the condition of the deceased was serious and that he had suffered from prolonged hypoxia, Hypercarbia and Hyperacidosis leading to all irreversible tissue damage including Brain and ultimately died in spite of intensive therapy.
Admittedly, there was no ventilator in
This indicates that the patient
suffered irreparable damage before he was shifted to
However, it is contended by the Respondents that the deceased developed fat embolism syndrome. For this purpose a reference is made to Review Article relevant portion whereof is as under:
The seriousness of fat embolism syndrome is not generally appreciated and the diagnosis is often overlooked. During the first week following major trauma, the causes of respiratory insufficiency include pulmonary contusions, fat embolic syndrome and shock lung.
The exact incidence and mortality of the syndrome is not known. The problem of fat embolism increase in direct proportion to the increase in automobile accidents. The greatest risk occurs with multiple fractures. Hoyt et al studied the incidence of pulmonary complications in trauma victims during a three year study period. They found that 11.2% of trauma patients developed fat embolism.
Onset of symptom is usually within 12 to 72 hrs, but may manifest as early as 6 hrs to as late as 10 days. The classic triad of fat embolism syndrome involves pulmonary changes, cerebral dysfunction and petechial rash.
Pulmonary findings usually are the earliest signs of the syndrome. Pulmonary insufficiency occurs in 75% of patients with fat embolism syndrome, and presents commonly as tachypnoea, dyspnoea and cyanosis. Rales and rhonchi can be heard. Hypoxaemia may be detected hours before the onset of respiratory symptoms. Approximately 10% of these patients progress to respiratory failure.
Treatment of Fat Embolism Syndrome
Careful monitoring of blood pressure, urinary output, and possibly pulmonary wedge pressure is helpful for management of shock. Over aggressive fluid resuscitation may worsen the patients pulmonary status ; if a perfusion can be maintained, judicious use of diuretic may be helpful. Analgesia often is overlooked in the treatment of fat embolism syndrome. Adequate analgesia is important to limit the sympathomimetic response to injury.
Respiratory support is the mainstay of the treatment of fat embolism syndrome. Early and frequent monitoring of respiratory function, either by pulse oximetry or arterial blood gases, is advocated for patients at risk of fat embolism syndrome. Respiratory support can range from the use of nasal canula to mechanical ventilation. Peltier suggested that immediate administration of oxygen (40%) via face mask or nasal canula may be all that necessary. However, if persistent worsening hypoxemia (PaO2<60 mmHg) and increasing respiratory distress are present despite supplemental oxygenation, then mechanical ventilation may be necessary. Continuous positive airway pressure (CPAP) may be helpful in avoiding mechanical ventilation. Positive end-expiratory pressure (PEEP) is advocated in conjunction with mechanical ventilation to avoid oxygen toxicity.
The most studied and most promising agents for the treatment of fat embolism syndrome are corticosteroids. Many studies have the beneficial effects of corticosteroids. The mechanism of action appears to be inhibition of the inflammatory reaction associated with fat embolism syndrome, including leucocyte aggregation, and a decrease in the rise of plasma free fatty acids levels. Corticosteroids appear to limit the decrease in PaO2 seen with fat embolism syndrome.
Morbidity and Mortality
Most commonly, fat embolism syndrome is self-limiting and pulmonary function returns to normal if adequate supportive care is given. Its mortality has decreased since the 1960s and 1970s, but it is thought that clinical fat embolism syndrome still has a mortality of 5% to 15%. Mortality is closely correlated with the degree of respiratory complications, which is the primary cause of death in most patients. Most long-term morbidity is secondary to focal cerebral neurologic deficits. The fulminant form of fat embolism syndrome still carried a higher mortality than does not clinically apparent fat embolism syndrome.
Fat embolism, usually subclinical, still occurs in the majority of patients with long bone fractures particularly of the femur and tibia. Despite certain laboratory and radiologic diagnostic aids, clinical diagnosis is still the cornestone of diagnosis of fat embolism syndrome. Respiratory insufficiency, central nervous system changes and petcchiae 1 to 2 days after injury is still considered pathognomic of fat embolism syndrome. Treatment consists of aggressive supportive care including fracture immobilization, respiratory support including possible mechanical ventilation, judicious volume replacement, analgesia, and corticosteroids in certain settings. Fortunately, most treated patients today survive fat embolism syndrome without sequelae.
From the aforesaid article it is clear
that even if there was a fat embolism syndrome, the mainstay of the
treatment for fat embolism, as stated above, is respiratory support,
which was not available in the
is undisputed that the deceased was admitted in
However, we direct the respondents to reimburse the complainants a sum of Rs. 4.00 lakhs ( Rupees Four lakhs) which they have spent for medical expenses including hotel expenses, travelling etc. The complaint is allowed to the aforesaid extent.
This award of compensation has nothing to do with the award of compensation for accident which may be passed under the M.A.C.T.
( M.B. SHAH)