Nipah virus encephalitis: A newly emerging disease

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The cause of death of three people, who were suffering from acute viral encephalitis, in Kozhikode has been confirmed to be due to the Nipah virus by the National Virology Institute in Pune.

Nipah and Hendra viruses are two related zoonotic pathogens that have emerged in the Asia-Pacific region. Both are RNA viruses that belong to the Paramyxoviridae family. The viruses jump the species barrier and infect a secondary animal host (e.g., pigs or horses), and transmit infections to humans

Here are some key facts about Nipah virus infection.

Nipah virus infection is a newly emerging zoonosis, which causes severe disease in both humans and animals. The associated mortality is high.
The natural hosts for the Nipah virus are the fruit bats of the Pteropus genus, which are symptomless carriers. Mainly four species have been demonstrated to have serologic evidence of infection with this virus. The virus is shed in the saliva, urine, semen and excreta of the infected bats.
Nipah virus spreads to humans through direct contact with infected bats, infected pigs, or other people who are infected with the virus. People have been also cautioned to avoid eating fruits that have fallen to the ground.
Nipah virus was first identified in 1998 as the cause of an outbreak of viral encephalitis among pig farmers in Malaysia, where pigs were the intermediate hosts. The virus derives its name from Sungai Nipah, a village in the Malaysian Peninsula where the pig farmers became ill with encephalitis. Since then, several outbreaks of acute Nipah encephalitis have been reported from Bangladesh, West Bengal (Siliguri), India with reports of person-to-person transmission in hospital settings and in the Southern Philippines. Raw date palm sap that had been contaminated by infected fruit bats was identified as the source of infection in an outbreak that occurred in Bangladesh in 2004.
The incubation period is 5 to 14 days.
Clinically, the main presentation of Nipah virus infection is as an encephalitic syndrome characterized by onset of non specific symptoms – sudden onset of fever, headache, myalgia, nausea and vomiting followed by drowsiness, disorientation and mental confusion. The infected person can become comatose within 24 to 48 hours.
The case fatality rate of Nipah encephalitis ranges from 9 to 75%
Meningismus is seen in approximately one-third of patients although marked nuchal rigidity and photophobia are uncommon.
Patients infected with Hendra virus have presented with fever and influenza like illnesses, or with meningoencephalitis
Nipah virus infection can be diagnosed by ELISA test.
On MRI, typically multiple, small (less than 5 mm), asymmetric focal lesions in the subcortical and deep white matter without surrounding edema are seen.
There is no effective treatment for Nipah virus infection. The mainstay of treatment is supportive care focusing on managing fever and the neurological symptoms. Infection control practices and barrier nursing are important as person-to-person transmission may occur. Severely ill patients need intensive care.
Ribavirin, a nucleoside analog, can be given empirically as it has a broad spectrum of antiviral activity against both RNA and DNA viruses. In the Malaysian outbreak, 140 treated patients were compared to 54 control patients who did not receive ribavirin. Fewer treated patients died (32% vs 54%). However, treated patients were identified later in the outbreak so it is possible that they were given better general medical care compared to untreated patients seen earlier. Subsequent animal models found that ribavirin, as well as chloroquine, were ineffective.
Anti-thrombotic agents, aspirin and pentoxyfylline, were administered in some patients based upon the recognition that arterial thrombosis may play an important role in the CNS disease.
Nipah virus is classified internationally as a biosecurity level (BSL) 4 agent. Biosafety Level 4 is required for work with dangerous and exotic agents that pose a high individual risk of aerosol-transmitted laboratory infections and life-threatening disease that is frequently fatal, for which there are no vaccines or treatments, or a related agent with unknown risk of transmission (CDC).

Surgery performed on the wrong patient is a never event

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A patient who was hospitalized in a dedicated Trauma Centre run by the Delhi government with head and face injuries that he sustained in an accident, instead underwent surgery under GA for a fractured leg, as reported in TOI. The surgeon mistook him for another patient admitted in the same ward who had a leg fracture. A small hole was drilled into the patient’s right leg to put a pin on Thursday morning. As the procedure had been done under general anesthesia, the patient could not realize or object to it. However, the pin was removed within hours following a corrective surgery after it was brought to the attention of the authoritis. A committee examined the case found merit in the allegations and a disciplinary action was initiated against the doctor, a senior resident, who has been barred from conducting surgeries without supervision with immediate effect.

Res ipsa loquitur is a Latin term, which literally translates as “the thing speaks for itself”. The doctrine of res ipsa loquitur is a rule of evidence in cases of medical negligence. It infers negligence from the very nature of an accident or injury in the absence of direct evidence on how any defendant behaved. Res ipsa loquitur is not applicable when determining the liability for criminal negligence; it applies only in cases of civil negligence.

To prove medical negligence, usually three components have to be established:

  1. There was an element of duty to be performed
  2. There was breach of duty
  3. Resultant damage

If the patient is not harmed by the physician’s error, then the patient cannot recover damages arising out of the error.

This case answers ‘yes’ to all the three components of medical negligence: there was a duty of care, there was a breach in the duty of care and the patient did suffer damage as a direct result of the breach.

In res ipsa loquitur, these three components of medical negligence elements are inferred from an injury that does not ordinarily occur without negligence i.e. negligence is evident and the complainant does not have to prove anything as the “thing proves itself” as also in this case.

This is a medical error and can be classified as a ‘never event’ i.e. event that should never occur under any circumstance. Never events are defined as adverse events that are serious, largely preventable, and of concern to both the public and health care providers for the purpose of public accountability. They are usually a direct result of a negligent action and no trial of expert’s evidence is necessary

The US National Quality Forum has defined 29 never events segregated into seven categories: surgical, product or device, patient protection, care management, environmental, radiologic, and criminal.

“Surgery or other invasive procedure performed on the wrong patient” is included in list of surgical never events along with “surgery or other invasive procedure performed on the wrong body part, wrong surgical or other invasive procedure performed on a patient, unintended retention of a foreign object in a patient after surgery or other procedure”.

The World Health Organization (WHO) has developed a Surgical Safety Checklist, to be read out loud, to decrease errors and adverse events for use in any operating theatre environment. The checklist has three phases as below:

“Sign In”Before induction of anesthesia

  1. Has the patient confirmed his/her identity, site, procedure and consent?
  2. Is the surgical site marked?
  3. Is the anaesthesia machine and medication check complete?
  4. Does the patient have a: Known allergy, Difficult airway/aspiration risk or Risk of >500ml blood loss (7ml/kg in children)?

An interpretation of medical report of the death of former Prime Minister Shri Lal Bahadur Shastri

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An interpretation of medical report of the death of former Prime Minister Shri Lal Bahadur Shastri

The death of former Prime Minister Shri Lal Bahadur Shastri, who passed away in Tashkent, then the Soviet Union on January 11, 1966 has always been surrounded by mystery and there are several conspiracy theories about his death.

Now 52 years after his death, the medical report of his death was revealed by the Govt. in reply to an RTI filed on 24.12.2017. The RTI had asked for information on the true cause/s of the death of the prime minister and asked for a certified copy of the postmortem conducted in the USSR/India. This information was provided in a reply dated 19.1.2018. The report is available at:(http://www.republicworld.com/india-news/general-news/government-of-india-reveals-the-exact-cause-of-death-of-former-prime-minister-lal-bahadur-shastri.

As per the medical report appended with the statement made by the then Minister of External Affairs in 1966, death of Shri Lal Bahadur Shastri occurred because of an acute attack of ‘Infarctmiocardia’.

I was asked by the media to comment on this report. I also spoke to top arrhythmia experts, who said that we have never used KCl in India. But, on searching PubMed, I could find some literature on the use of KCl in cardiac arrest. May be this was the standard protocol followed by doctors in USSR at that point of time, which also correlates with scientific evidence.

Here is my interpretation (right of the box) of the medical report of the death of the former Prime Minister of India Shri Lal Bahadur Shastri.

During all the days of his stay in Tashkent, as well as on evening of January 1966, the Prime Minister of India Lal Bahadur Shastri felt well. He never complained about his health.
On the evening of 10th January 1966, the prime minister of India, Lal Bahadur Shastri as healthy and cheerful while he was attending a reception given by the chairman of the council of ministers of USSR, AN Kosygin.
According to Dr RN Chugh, the doctor-attendant on the Prime Minister, who used to be always present at his side and thus had attended the reception, after return from the reception to his residence, Lal Bahadur Shastri was in normal health and was in a good mood and spoke over the telephone with his relatives in Delhi. He went to bed at about 12:30 midnight.
On the 11th of January, at about 1.20 in the morning, Messrs, Shay, Kapur and Sharma approached the Premier’s doctor who was in the room next to him and told him that the Prime Minister is feeling unwell. He became unwell at 1.20 am
Dr R N Chugh at once approached the Prime Minister and found that the Prime Minister was sitting on his bed, coughing and was complaining of lack of breath. He was holding his chest with his hands and looking pale. The doctor found the pulse to be very fast and blood pressure was not registered. The heart beats were hardly audible. This is a classical presentation of acute heart attack with left ventricular failure. Ventricular arrhythmia can be a possibility.
With the help of gentlemen mentioned above the doctor put the Prime Minster in the reclining position, gave him intramuscular injection of MEPHENTINE SULPHATE one ml (15 milligram) and 1 ml of MICOREN. At that point of time, mephenteramine was a common drug given to raise the blood pressure. Micorena was a respiratory stimulant.
Within the next 3 minutes, PRIME MINISTER LB Shastri lost consciousness, the pulse disappeared, and breathing stopped and heart rate could not be heard. It was a cardiac arrest.
Death occurred at 1.32 am in the morning of 11th January 1966.
Doctor R. N. Chugh had already began revival treatment by the method of indirect message of the heart and artificial respiration through the mouth by means of the air tube. CPR was attempted.
The soviet doctor V G VERMENKO who had come there immediately on a call from Dr RN Chugh also took part in the treatment by revival procedure.

She found Prime Minister LB Shastri dead when she arrived. The pulse had stopped, the heart was silent, there was no breath and no corneal reflexes. The revival was continued further with the help of anti-….team of doctors which had arrived immediately on call.

Indirect massage of the heart was done, in the left cavity mixture of potassium chloride with adrenaline and glucose Here is some literature on the use of KCl in cardiac arrest.

Romain Jouffroy and Benoît Vivien. Antiarrhythmic drugs in out-of-hospital cardiac arrest: is there a place for potassium chloride? Crit Care. 2017;21 144.

According to current guidelines, antiarrhythmic drugs should be administered during the metabolic phase of cardiac arrest, which is paradoxically the most unfavorable phase for their efficiency [1]. Twenty-five years ago, Beyersdorf et al. [2] observed that administration of a high-potassium solution could salvage cardiac arrest patients due to an irreversible VF in metabolic phase of cardiac arrest. Direct intravenous KCl injection was recently shown efficient to stop refractory VF in a patient under continuous ECLS: a few minutes after KCl administration, the heart recovered a hemodynamically efficient normal sinus rhythm [3].

1.    Soar J, Nolan JP, Bottiger BW, et al. European Resuscitation Council Guidelines for Resuscitation 2015: Section 3. Adult advanced life support. Resuscitation. 2015;95:100–47. doi: 10.1016/j.resuscitation.2015.07.016. [PubMed] [Cross Ref]

2.    Beyersdorf F, Kirsch M, Buckberg GD, et al. Warm glutamate/aspartate enriched blood cardioplegic solution for perioperative sudden death. J Thorac Cardiovasc Surg. 1992;104(4):1141–7.[PubMed]

3.    Jouffroy R, Lamhaut L, Philippe P, et al. A new approach for treatment of refractory ventricular fibrillation allowed by extra corporeal life support (ECLS)? Resuscitation. 2014;85(8):e118. doi: 10.1016/j.resuscitation.2013.12.038. [PubMed] [Cross Ref]

Metabolic phase is defined as greater than 10 minutes of pulselessness. It is primarily based upon post-resuscitative measures, including hypothermia therapy. If not quickly converted into a perfusing rhythm, patients in this phase generally do not survive.

Refractory cardiac arrest is defined as the absence of return of spontaneous circulation (ROSC) after 30 min of cardiopulmonary resuscitation (CPR).

Jouffroy R, Lamhaut L, Philippe P, An K, Carli P, Vivien B. A new approach for treatment of refractory ventricular fibrillation allowed by extra corporeal life support (ECLS)? Resuscitation. 2014;85(8):e118.

A 50-year-old male with refractory ventricular fibrillation (VF) out-of-hospital cardiac arrest (OHCA) was treated at home by a mobile intensive care unit team. Since ROSC was not achieved after 30 min of prehospital resuscitation despite 20 external shocks and 900 mg IV amiodarone, the patient was admitted to an ICU for implementation of ECLS (Cardiohelp Maquet©), which was started with an initial rate of 4 l min−1 (4000 rev min−1), resulting in a mean arterial blood pressure of 65 mmHg. However, VF persisted despite five additional shocks.  Since adequate tissue perfusion was ensured by ECLS, potassium chloride 3 g was injected intravenously in order to stop the VF. Less than 1 min later, the patient presented with a stable sinus cardiac rhythm, and progressively recovered spontaneously efficient circulatory function. Coronary angiography revealed an occlusion of the right coronary artery, which was treated by angioplasty and endovascular stent implementation. ECLS was removed on day 2 and the patient weaned from mechanical ventilation on day 6, and discharged on day 11 with a cerebral performance category (CPC) score of 2.

The use of potassium to treat persistent VF has been described during cardiothoracic surgery6 and in a pig model of cardiac arrest,7 but to the best of our knowledge, our case is the first to describe potassium administration to stop refractory VF, while effective tissue perfusion was ensured using ECLS. Further studies are required to evaluate the efficiency of this treatment for patients in refractory VF treated with ECLS.

1.     Le Guen, M., Nicolas-Robin, A., Carreira, S. et al. Extracorporeal life support following out-of-hospital refractory cardiac arrest. Crit Care. 2011; 15: R29.

2.     Cave, D.M., Gazmuri, R.J., Otto, C.W. et al. Part 7: CPR techniques and devices: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2010; 122: S720–S728.

3.     Neumar, R.W., Otto, C.W., Link, M.S. et al. Part 8: adult advanced cardiovascular life support: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2010; 122: S729–S767.

4.     Van Alem, A.P., Post, J., and Koster, R.W. VF recurrence: characteristics and patient outcome in out-of-hospital cardiac arrest. Resuscitation. 2003; 5: 181–188.

5.     Liu, Y., Zhang, S.L., Duan, W.X. et al. The myocardial protective effects of a moderate-potassium blood cardioplegia in pediatric cardiac surgery: a randomized controlled trial. Ann Thorac Surg. 2012;94: 1295–1301.

6.     Watanabe, G., Yashiki, N., Tomita, S., and Yamaguchi, S. Potassium-induced cardiac resetting technique for persistent ventricular tachycardia and fibrillation after aortic declamping. Ann Thorac Surg. 2011; 91: 619–620.

7.     Lee, H.Y., Lee, B.K., Jeung, K.W. et al. Potassium induced cardiac standstill during conventional cardiopulmonary resuscitation in a pig model of prolonged ventricular fibrillation cardiac arrest: a feasibility study. Resuscitation. 2013; 84: 378–383.

Artificial respiration by means of the machines with the help of intubation tube was also attempted.

However, those measures yielded no results.

The following professors also took part in the entire treatment

UA ARIPOV

YK GORDAN

ON PAVLON

AR RAKHIMJANOY

MS THRSUM-KHOJAEVA

ZE UMMIDOVA

19.1.18

Praveen Kumar

PMO

Sd/-
RRTI /5510/2017/PMR Rohit Chaudhury

Dr KK Aggarwal

Padma Shri AwardeeVice President CMAAOGroup Editor-in-Chief IJCP Publications

President Heart Care Foundation of India

Immediate Past National President IMA

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