A case report describes the improvement of a critically ill patient with H1N1 ‘flu after the administration of N-acetylcysteine in a dose similar to that used to treat paracetamol (acetaminophen) overdose.
Influenza virus induces reactive oxygen species that activate nuclear factor kappa B to produce cytokines. High-dose N-acetylcysteine, an antioxidant, is thought to reduce the production of this cytokine storm which contributes to the lethality of influenza. More studies are clearly needed.
High-Dose N-Acetylcysteine Therapy for Novel H1N1 Influenza Pneumonia
Ann Intern Med. 2010 May 18;152(10):687-8
Category Archives: ICU
Stuff relevant to patients on ICU
What fluid in rhabdomyolysis?
A ‘BestBET‘ from the Emergency Medicine Journal examined the evidence for the use of sodium bicarbonate and/or mannitol in the management of rhabdomyolysis.
The clinical bottom line: there is no quality published evidence that alkaline diuresis is a superior treatment to normal saline alone.
Rhabdomyolysis and the use of sodium bicarbonate and/or mannitol
Emerg Med J. 2010 Apr;27(4):305-8
Full Text at the BestBets site
Misoprostol for PPH
Misoprostol is a prostaglandin analogue with uterotonic activity. It was compared with placebo in its sublingual form in a randomised trial in 1422 women with postpartum haemorrhage and uterine atony. It was given with other uterotonic agents (mostly oxytocin 10IU im or slow iv). The primary outcome was blood loss of 500 mL or more within 60 min after randomisation, and this was similar in both groups.
Misoprostol as an adjunct to standard uterotonics for treatment of post-partum haemorrhage: a multicentre, double-blind randomised trial
Lancet. 2010 May 22;375(9728):1808-13
Lung Ultrasound Articles
Here are some sites that explain lung sonography as applied to critical care patients:
Clinical review: Bedside lung ultrasound in critical care practice – Critical Care Full Text
Evaluation of ultrasound lung comets by hand-held echocardiography – Cardiovascular Ultrasound Full Text
ICU Sonography Site – Lung Ultrasound Tutorial
Terlipressin for refractory cardiac arrest in kids
Okay so it’s a small case series – but the results warrant further investigation: 10-20 mcg/kg terlipressin was given to five infants and children who arrested in the paediatric intensive care unit and who had not responded to several doses of adrenaline (epinephrine)1. Sustained return of spontaneous circulation (ROSC) was achieved in four, and two survived to be discharged home without sequelae and with good neurologic status at 6 and 12 month follow up. Interestingly, the four patients who had ROSC all had septic shock as the cause of their arrest. The two survivors had severe bradycardia and severe bradycarda-asystole as the arrest rhythms, and both received 20 mcg/kg terlipressin.
Terlipressin is a synthetic arginine vasopressin analog with a significantly longer duration of effect, which previously showed positive effects when administered to a small group of children unresponsive to prolonged resuscitative efforts2.
1. Pediatric cardiac arrest refractory to advanced life support: Is there a role for terlipressin?
Pediatr Crit Care Med. 2010 Jan;11(1):139-41
2. Beneficial effects of terlipressin in prolonged pediatric cardiopulmonary resuscitation: A case series.
Crit Care Med. 2007 Apr;35(4):1161-4
Paediatric Retrieval – what's the rush?
The Children’s Acute Transport Service (CATS) in the UK performed 2106 interfacility transports between April 2006 and March 2008. The stabilisation time averaged just over 2 hrs. Stabilisation time was prolonged by the number of major interventions required to stabilise the patient before transfer and differed significantly between various diagnostic groups. The length of time spent by the retrieval team outside the intensive care environment had no independent effect on subsequent patient mortality.
They have shown that stabilisation time can be influenced by a number of patient- and transport team-related factors, and that time spent undertaking intensive care interventions early in the course of patient illness at the referring hospital does not increase patient mortality. In the authors’ words: ‘the “scoop and run” model can be safely abandoned in favor of early goal-directed management during interhospital transport for intensive care.‘
There’s NO rush guys!
Effect of patient- and team-related factors on stabilization time during pediatric intensive care transport
Pediatr Crit Care Med. 2010 May 6
Control oxygenation after resuscitation
How much oxygen should we give patients after successful cardiac arrest resuscitation? Too little oxygen may potentiate anoxic injury. Too much oxygen may increase oxygen free radical production, possibly triggering cellular injury and apoptosis. A multicentre ICU database of over 6300 post-arrest patients was analysed and demonstrated an association between ‘hyperoxia’ and in-hospital mortality.
Adult patients who sustained nontraumatic cardiac arrest and were admitted to the ICU at a participating center between 2001 and 2005 were included. Specifically, inclusion criteria were age older than 17 years, nontraumatic cardiac arrest, cardiopulmonary resuscitation within 24 hours prior to ICU arrival, and arterial blood gas analysis performed within 24 hours following ICU arrival.
The cohort was divided into 3 exposure groups defined a priori based on PaO2 on the first arterial blood gas values obtained in the ICU. Hyperoxia was defined as PaO2 of 300 mm Hg (39.5 kPa) or greater; hypoxia, PaO2 of less than 60 mm Hg (7.9 kPa) (or ratio of PaO2 to fraction of inspired oxygen [FIO2] <300); and normoxia, cases not classified as hyperoxia or hypoxia.
Exposure to hyperoxia was found to be a significant predictor of in-hospital death (OR, 1.8 [95% CI, 1.5-2.2]; this was an independent effect that persisted after adjusting for all other significant risk factors
The authors acknowledge that association does not necessarily imply causation, but add that these data support the hypothesis that high oxygen delivery in the postcardiac arrest setting may have adverse effects.
Association Between Arterial Hyperoxia Following Resuscitation From Cardiac Arrest and In-Hospital Mortality
JAMA. 2010;303(21):2165-2171
Post cardiac arrest guideline
A patient is resuscitated from an out-of-hospital cardiac arrest and is in your emergency department, comatose, with a pulse.
You know that therapeutic hypothermia is indicated and are happy with the protocol for that. You clinically assess for the underlying cause with history, examination, ECG, and other investigations as indicated.
Someone asks you if you want to give some magnesium “as per the guidelines”. As you are wondering what that’s for someone else asks you how long myocardial stunning lasts for and whether that’s the likely cause of hypotension now.
Luckily you avoid getting annoyed with all these reasonable questions by suddenly remembering that there are international recommendations for the management of ‘Post–Cardiac Arrest Syndrome’. You excuse yourself from the room on the pretext of going to the lavatory and quickly find a quiet area where you scan the following article for help:
Post–Cardiac Arrest Syndrome Epidemiology, Pathophysiology, Treatment, and Prognostication
A Consensus Statement From the International Liaison Committee on Resuscitation (American Heart Association, Australian and New Zealand Council on Resuscitation, European Resuscitation Council, Heart and Stroke Foundation of Canada, InterAmerican Heart Foundation, Resuscitation Council of Asia, and the Resuscitation Council of Southern Africa); the American Heart Association Emergency Cardiovascular Care Committee; the Council on Cardiovascular Surgery and Anesthesia; the Council on Cardiopulmonary, Perioperative, and Critical Care; the Council on Clinical Cardiology; and the Stroke Council
Circulation 2008;118;2452-2483 Full Text Article
Guidelines for Clostridium Difficile
Guidelines for preventing, detecting, and treating Clostridium Difficile infection from the Infectious Diseases Society of America have been published.
Clinical Practice Guidelines for Clostridium difficile Infection in Adults: 2010 Update by the Society for Healthcare Epidemiology of America (SHEA) and the Infectious Diseases Society of America (IDSA)
Infect Control Hosp Epidemiol 2010;31:431–455 Full Text
PCI and therapeutic hypothermia
Percutaneous coronary intervention did not increase the risk of dysrhythmia, infection, coagulopathy, or hypotension associated with therapeutic hypothermia after cardiac arrest. Intensivists and cardiologists should perhaps agree that this adds to existing evidence that the two therapies are not mutually exclusive.
Feasibility and safety of combined percutaneous coronary intervention and therapeutic hypothermia following cardiac arrest
Resuscitation. 2010 Apr;81(4):398-403