UMEM Educational Pearls - By Zach Rogers

Prophylactic antibiotic use in cirrhotic patients with an upper GI bleed has been demonstrated to have a mortality benefit in multiple randomized clinical trials. Some trials as well demonstrated a decreased risk of rebleeding as well as a shorter hospital length of stay (1,2).

The exact means of protection is not entirely clear and its benefit is seen in both variceal and nonvariceal hemorrhages as well as in cirrhotic patient both with and without ascites.

There does appears to be a close interplay between cirrhosis bleeding risk and infection, with infection being a common precipitating factor for upper GI bleed.

The antibiotic of choice is ceftriaxone 1 gram IV daily for seven days. Although in case of allergy/intolerance, fluoroquinolones or aminoglycosides may be used as alternatives (3).

Bottom line:

All forms of upper GI hemorrhage in cirrhotic patients warrant prophylactic antibiotic use (regardless of the presence of ascites) as well as a diligent search and exclusion of possible infectious sources.

 

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Glucagon therapy in beta blocker and calcium channel blocker overdose is controversial and no high level evidence is available to support or refute its use in overdose treatment.

Glucagon has the ability to bypass adrenergic blockade from beta and calcium channel blocking agents and theoretically increase myocardial contraction, increase heart rate, and increase AV conduction through cyclic AMP production.

However, practically, the use of glucagon is limited due to high risk of vomiting and subsequent risk of aspiration with administration as well as the high cost and limited hospital stock available for continued use.  

Given these limitations, glucagon therapy is no longer recommended for calcium channel blocker overdose in the 2017 Critical Care Medicine Expert Consensus*. The use in beta blocker therapy is still recommended. However, caution must be taken to ensure that more advanced (and possibly more efficacious) therapies such as vasopressors and high dose insulin are administered without delay.

The dose of glucagon therapy for this indication is 3-10 mg IV. You can repeat this dose a second time if no response is seen with the first dose. If clinical response is seen with bolus dosing, transition to continuous infusion at the dose of clinical response (eg. if two 5 mg boluses produced the desired response; start 10 mg/hr infusion). Antiemetic administration prior to initial bolus dose is highly recommended to avoid vomiting.

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Sympathetic Crashing Acute Pulmonary Edema (SCAPE) (also known as flash pulmonary edema) is an extreme form of hypertensive acute heart failure where a surge of high blood pressure from catecholamine surge and sudden vascular redistribution causes sudden onset decompensated heart failure hallmarked by rapid pulmonary edema and symptoms of hypoxia and dyspnea.

This is treated by systolic blood pressure control and venous vasodilation with IV nitroglycerine, bilevel positive airway pressure (BPAP), and diuretics if needed. A common error in treatment is administration of the traditional IV nitroglycerine infusion dosing protocol in which the nitroglycerine infusion is started at 5 mcg/min and slowly increased by 5 mcg/min increments until the clinical response is seen. However, in this syndrome, rapid blood pressure control and correction of vascular redistribution is critically important to reverse the central factor for patient decompensation. Lack of blood pressure control places the patient at risk of further cardiac decompensation or respiratory failure ultimately requiring intubation.

Increasing literature has been published on the concept of high dose or push dose IV nitroglycerine for the treatment of this syndrome. Many of these studies show decreased rates of intubation, decreased ICU admissions, and shorter hospital length of stays with high dose or push dose nitroglycerine, while also demonstrating low risk of hypotension.

The actual dose of the high-dose nitroglycerine administered in these trials is variable, with some trials administering nitroglycerine 1-2 mg IV pushes every 3-5 minutes, and other trials using a nitroglycerine infusion at a much higher starting rate (between 200-400 mcg/min) with rapid down-titration as blood pressure is controlled.

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Thrombolytic-induced angioedema is a known complication of alteplase or tenecteplase administration, occurring in 0.9-5.1% of patients who received thrombolytics due to ischemic stroke. Angioedema occurs due to activation of the kinin and complement pathway by plasminogen, leading to both bradykinin and histamine release.

Swelling most commonly occurs acutely while the t-PA is infusing, but can have a delayed presentation up to 24 hours post administration. It normally has an orolingual distribution, although in severe cases there can be laryngeal involvement as well. There is a 4-fold-increase occurrence in patients who take ACE inhibitor medications ^[1] with some studies noting a high prevalence in strokes involving the right insular brain region ^[2].

Once identified, the t-PA infusion should be immediately discontinued. As there may be histamine involvement in angioedema formation, patients are initially treated with steroids, H1, and H2 blockers with as needed epinephrine injections.

Given the orolingual predominance, airway obstruction must be ruled out and the patient closely monitored with emergent intubation performed if necessary.

As the kinin pathway (bradykinin) appears to play the largest role in angioedema formation, C1 esterase inhibitors and bradykinin inhibitors can be used in severe or refractory cases ^[3,4].

However, most cases are mild and resolve with t-PA discontinuation and the initial steroid and histamine blockade.

 

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Question

Arterial line waveform interpretation and troubleshooting are essential skills for any physician caring for critically ill patients. Overdamping and underdamping of the arterial line waveform leads to inaccurate systolic and diastolic blood pressure readings which can lead to unidentified hypertension or hypotension. In addition to scrutiny of the arterial waveform pattern, the square-wave test is a tool to identify overdamped or underdamped arterial lines. 

Overdamped arterial waveforms will underestimate systolic blood pressure and overestimate diastolic blood pressure. Underdamping will have the opposite effect and overestimate systolic blood pressure and underestimate diastolic blood pressure. In both cases, the mean arterial pressure (MAP) often remains the same.  

The square-wave test is a rapid flush that is applied to the arterial line for approximately 1 second. This rapid high-pressure surge results in vibration and oscillation of the arterial catheter. These oscillations are then read by the pressure transducer and the number and amplitude of these oscillations can be measured. 0 or 1 oscillations is suggestive of overdamping. 3 or more oscillations is suggestive of an underdamped system. 

Major causes of an overdamped arterial line waveform include low infusion bag pressure, loose connectors, air bubbles in the tubing, blood clot in the circuit, or kinking of vascular catheter. An underdamped arterial line, however, is caused by overly stiff circuit tubing or a defective transducer.   

 

Scrutiny of the arterial waveform and utilization of the square-wave test can be helpful to both identify erroneous arterial line blood pressure readings as well as suggest likely corrective measures.  

 

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Question

Traditionally, internal jugular and subclavian central line placement has required chest x-ray confirmation of correct placement (venous cavoatrial junction placement) as well as demonstrating lack of complication (no pneumothorax) prior to use of that central line. However, current evidence supports similar if not superior complication identification and placement confirmation with ultrasound,^(1-7) allowing for a much quicker confirmation time than traditional chest x-ray, which can be vital in critically ill patients who need immediate medication administration.

Venous placement is confirmed with prompt visualization of microbubbles in the right atrium and ventricle with a rapid flush of 5-10 ml of agitated saline via the distal central line port. Additionally, if the opacification occurs <2 seconds after injection then the catheter tip is sufficiently distal in the central venous system to not require additional verification. Additional confirmation of lung sliding in both lung apices will rule out pneumothorax.

Some authors recommend checking the contralateral internal jugular vein to ensure that the central line catheter has not traveled up the internal jugular towards the head, however this may be redundant as long as the time from agitated saline injection to right atrial visualization of microbubbles is clearly less than 2 seconds.

Bottom Line: Utilization of ultrasound for central line placement confirmation is a relatively simple, rapid, safe, and accurate means of confirmation of venous catheter placement and catheter tip location, as well as ruling out pneumothorax complications.

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