Q: Give one non-infectious condition which can be treated by IV penicillin G?

Hint: It is use as an antidote.

Answer: A phalloides mushroom intoxication

There is no definitive antidote available for a phalloides mushroom intoxication, but high-dose continuous intravenous penicillin G has been reported to help but the exact mechanism is unknown.

Another useful treatment is said to be intravenous silibinin.

As with other toxin gastric decontamination with either activated carbon or gastric lavage should be done. Also like in other hepatic conditions associated with toxin ingestions N-acetylcysteine should also be used. Liver transplant team should be involved too.

Q: 52 year old alcoholic male who is frequent flyer at your ED presents again with symptoms of Wernicke encephalopathy. Despite quick repletion of Thiamine upto 300 mg IV - symptoms persist. What could be the missing point?



Answer: Hypomagmesemia

Patients with Wernicke encephalopathy may not response to parenteral thiamine in the presence of low magnesium level. Once magnesium is repleted thiamine will have effect, the blood transketolase activity will return to normal and clinical symptoms will resolve.

Please request pharmacy to provide fresh Thiamine solution, since old solutions quickly get inactive.

Merci Clot Retrieval Animation in CVA

(2 videos)

Learn about the Merci Retrieval System

Gadolinium, MRIs, Renal failure and Nephrogenic systemic fibrosis

Nephrogenic systemic fibrosis (NSF) is a rare but a serious disease that involves fibrosis of skin, joints, eyes, and internal organs. It is found to be associated with exposure to gadolinium for MRIs in patients with severe kidney failure. It can happen anywhere from few hours to months after exposure.

NSF is a clinical and histopathological diagnosis. Most patients with NSF require quick diagnosis and aggressive hemodialysis. Gadolinium-containing contrast is now considered relatively contraindicated in patients with an estimated GFR under 60 and especially under 30 ml/mn.

Not all but 4 of the 7 gadolinium contrast agents have been implicated in NSF.

End of Life Care!

Background: Little information exists about the expected time to death after terminal withdrawal of mechanical ventilation. We sought to determine the independent predictors of time to death after withdrawal of mechanical ventilation.

Methods: We conducted a secondary analysis from a cluster randomized trial of an end-of-life care intervention. We studied 1,505 adult patients in 14 hospitals in Washington State who died within or shortly after discharge from an ICU following terminal withdrawal of mechanical ventilation (August 2003 to February 2008). Time to death and its predictors were abstracted from the patients’ charts and death certificates. Predictors included demographics, proxies of severity of illness, life-sustaining therapies, and International Classification of Diseases, 9th ed., Clinical Modification codes.

Results: The median (interquartile range [IQR]) age of the cohort was 71 years (58-80 years), and 44% were women.

The median (IQR) time to death after withdrawal of ventilation was 0.93 hours (0.25-5.5 hours).

Using Cox regression, the independent predictors of a shorter time to death were

• nonwhite race (hazard ratio [HR], 1.17; 95% CI, 1.01-1.35)
• number of organ failures (per-organ HR, 1.11; 95% CI, 1.04-1.19),
• vasopressors (HR, 1.67; 95% CI, 1.49-1.88), IV fluids (HR, 1.16; 95% CI, 1.01-1.32), and
• surgical vs medical service (HR, 1.29; 95% CI, 1.06-1.56).

Predictors of longer time to death were

• older age (per-decade HR, 0.95; 95% CI, 0.90-0.99) and
• female sex (HR, 0.86; 95% CI, 0.77-0.97).

Conclusions: Time to death after withdrawal of mechanical ventilation varies widely, yet the majority of patients die within 24 hours. Subsequent validation of these predictors may help to inform family counseling at the end of life.

Predictors of Time to Death After Terminal Withdrawal of Mechanical Ventilation in the ICU - CHEST August 2010 vol. 138 no. 2 289-297

19% of PFOs in ARDS!

Objective: Right-to-left shunting across a patent foramen ovale may occur in acute respiratory distress syndrome as a result of pulmonary hypertension and positive-pressure mechanical ventilation. The shunt may worsen the hypoxemia. The objective of our study was to determine the prevalence, clinical implications, and prognosis of patent foramen ovale shunting during acute respiratory distress syndrome.

Design: Prospective study of 203 consecutive patients with acute respiratory distress syndrome.

Interventions: Patent foramen ovale shunting was detected by using transesophageal echocardiography with modified gelatin contrast. Moderate-to-large shunting was defined as right-to-left passage of at least 10 bubbles through a valve-like structure within three cardiac cycles after complete opacification of the right atrium. In 85 patients without and 31 with shunting, the influence of the positive end-expiratory pressure level on shunting was studied.

Measurements and Results:

• The prevalence of moderate-to-large patent foramen ovale shunting was 19.2% (39 patients).
  
• Compared to those in the group without shunting, the patients in group with shunting had larger right ventricle dimensions, higher pulmonary artery systolic pressure, and a higher prevalence of cor pulmonale.
  
• Compared to patients without shunting, patients with shunting had a poorer Pao₂/Fio₂ ratio response to positive end-expiratory pressure, more often required prone positioning and nitric oxide as adjunctive interventions, and had fewer ventilator-free and intensive care unit-free days within the first 28 days.

Conclusions: Moderate-to-large patent foramen ovale shunting occurred in 19.2% of patients with acute respiratory distress syndrome, in keeping with findings from autopsy studies. Patent foramen ovale was associated with a poor oxygenation response to positive end-expiratory pressure, greater use of adjunctive interventions, and a longer intensive care unit stay.

Prevalence and prognosis of shunting across patent foramen ovale during acute respiratory distress syndrome -Critical Care Medicine: September 2010 - Volume 38 - Issue 9 - pp 1786-1792