Vesta’s E-shift

1. What is the incidence of SBP in hospitalized patients with liver cirrhosis? What are the causes?

SBP is a frequent complication of liver cirrhosis. It occurs in about 30% of hospitalized patients with liver cirrhosis (http://www.hepatitisc.uw.edu/go/management-cirrhosis-related-complications/spontaneous-bacterial-peritonitis-recognition-management/core-concept/all). It has an in-hospital mortality rate of about 33% and a 4 month follow up out of hospital mortality of 54% in one study (http://www.ncbi.nlm.nih.gov/pubmed/10413915). It is often due to the passage of intestinal bacteria into the lymph vessels, systemic circulation and ascitic fluid. Its incidence depends on the severity of liver failure and portends a poor prognosis. Anterior gastrointestinal hemorrhage, amount albumin in ascitic fluid, high bilirubin levels and patients with prior history of SBP are predictive factors for the development of SBP (http://www.ncbi.nlm.nih.gov/pubmed/10413915) Short term and long term prophylaxis with PO antibiotics is effective in preventing bacterial infections (http://www.ncbi.nlm.nih.gov/pubmed/7843826).

2. How is hepatic encephalopathy acutely treated in the ED?

Hyperammonemia is thought to play a role in hepatic encephalopathy (HE). Hyperammonemia can precipitate cerebral edema, intracranial hypertension and ultimately hypoxic brain injury. Lactulose if frequently used to treat HE. Some studies show it is associated with improved survival time but not necessarily with improvement of neurological status while some other studies show the reverse. Antibiotics such as neomycin are also commonly used with some sources saying it has perhaps more efficacy than lactulose. Unlike the usual management of seizures, seizure in patients with HE should be treated primarily with phenytoin to prevent a benzo oversedation secondary to decreased hepatic metabolic capabilities. Intracranial hypertension (as evidenced by neurological signs with hyperammonemia) should be treated by elevating the head of the bed 30 degrees and giving a bolus of mannitol 0.5-1.0g/kg. This decreases ICP and improves survival in this patient population.

3. How much blood can hemoccult test detect? How much blood is required to produce melena?

The hemoccult FOBT can detect as little as 7mg blood per 1g of stool. GI losses of as little as 10cc/day can and should give rise to a positive Hemoccult test. Because blood loss can be intermittent in some case, several samples and different times should be obtained especially if laboratory or clinical suspicion indicates. Keep in mind that hemoccult testing is less sensitive in upper GI bleeds as the specimen may be more diluted with other contents plus degraded to the point that it expels the heme and free heme is less reactive (Blood: Principles and Practice of hematology by R. Handin). A minimum of about 50-100cc of blood is required to produce melena furthermore the bleeding has to be fairly rapid, so if melena is detected a much more significant bleed has occurred (Clinical Diagnosis for Medical Undergraduates by Shaila Palekar)

Fahad’s July E-shift

1. Does using 2% lidocaine offer any advantage over using 1% lidocaine?

Per Up-to-date, and Roberts and Hedges, higher concentrations of lidocaine beyond 1% do not improve the onset, or the duration of analgesia, and may increase the risk of toxicity. As for toxic doses of lidocaine, they are not to exceed 7mg/kg (0.7 ml/Kg, or maximum of 500mg), when used with epinephrine, and 4mg/kg without epinephrine.

So what are your options if increased onset or duration of analgesia is desired?

One simple approach would be using lidocaine with epinephrine, as that would allow you to use a higher dose of lidocaine without reaching toxic levels. This is particularly advantageous when anesthetizing for laceration repairs in areas that are highly vascular, such as the face. Lidocaine with epinephrine has a more prolonged duration of action when compared to lidocaine alone.

Additionally, other anesthetics such as bupivacaine, mepivacaine, and/or procaine can also be employed, as it has a longer duration of action. This may be more useful in doing nerve blocks to treat dental pain, for example, where the goal is prolonged analgesia until ideally definitive care is sought.

Comparison of commonly infiltrated local anesthetics

Infiltration anesthetic	Concentration (percent)	Physiochemical properties				Maximum allowable dose*		Maximum total dose*
		Lipid:water solubility	Relative potency	Onset of action (min)	Duration (min)	mg/kg	mL/kg	mgequivalent solution volume
Lidocaine
Without epinephrine	1	2.9	2	2-5	50-120	4-5	0.4-0.5	30030 mL of 1 percent
With epinephrine (1:200,000)	1	2.9	2	2-5	60-180	5-7	0.5-0.7	50050 mL of 1 percent
Mepivacaine
Without epinephrine	1	0.8	2	2-5	50-120	5	0.5	30030 mL of 1 percent
With epinephrine•(1:200,000)	1	0.8	2	2-5	60-180	5-7	0.5-0.7	50050 mL of 1 percent
Bupivacaine
Without epinephrine	0.25	27.5	8	5-10	240-480	2	0.8	17570 mL of 0.25 percent
With epinephrine (1:200,000)	0.25	27.5	8	5-10	240-480	3	1.2	22590 mL of 0.25 percent
ProcaineΔ	1	0.6	1	5-10	60-90	7-10	0.7-1	50050 mL of 1 percent

 

2. How should you reverse Coumadin toxicity in a patient with a mechanical heart valve?

The risk of major bleeding has to be weighed against that of valve thrombosis.

If the patient is not bleeding and has an INR of >6, Coumadin can be temporarily discontinued, with small doses of oral vitamin k. With an INR of >10 and no bleeding, higher doses (2-5 mg) of oral vitamin k can be used with close INR monitoring.

If the patient is bleeding, and the bleeding is inaccessible to local control (i.e. intracranial hemorrhage), FFP along with 2.5 to 5 mg of vitamin k should be used. With major bleeding, intravenous unactivated prothrombin complex concentrates (PCC) and low-dose oral or IV vitamin K can be used, with repeated doses of vitamin k at 12 hour intervals. PCC is preferred over fresh frozen plasma, where available.

Recombinant factor 7 is not recommended, as there is insufficient evidence for its efficacy in Coumadin reversal. A study done in the journal Blood in 2010 showed that in healthy subjects showed that while factor 7 reduced the INR, it did not decreased the bleeding in a skin punch biopsy model.

3. Is there a role for urinary amylase in the diagnosis of acute pancreatitis? 

Plasma amylases can enter the urine through glomerular filtration. Conditions that cause increased entry of amylase into plasma (eg, acute pancreatitis) will thus result in increased urinary excretion of amylase. Urinary amylase clearance is increased about 3-fold for 1 to 2 weeks in patients with acute pancreatitis. A value > 550 U/L has been reported as 62% sensitive and 97% specific for acute pancreatitis, while a value > 2000 U/L has been reported as 62% sensitive and 97% specific for acute pancreatitis. Urinary amylase is therefore sometimes used in the diagnosis of acute pancreatitis. However, the rate of urinary amylase excretion appears to be less sensitive than plasma markers, and is not specific for the diagnosis of acute pancreatitis.