Archive | June, 2012

Desmopressin (DDAVP) and Bleeding

29 Jun


You have a hemodialysis patient present with altered mental status and hematemesis.  He is found to be in metabolic disarray including acute on chronic renal failure.  You admit him to the MICU and consult the renal fellow, who advises you to start DDAVP. Why?


DDAVP is a synthetic analogue of antidiuretic hormone that was initially designed to treat Diabetes Insipidus.

In the 1970s, studies showed that it also increases Factor VIII and von Willebrand Factor and its use was expanded to assist in treatment of Hemophilia A and von Willibrand’s disease.  Since then, it’s use has been expanded to various bleeding conditions (congenital and acquired).

The exact mechanism of bleeding in uremic patients it unknown, but seems to be multifactorial.  Advantages of DDAVP include short time to onset of action, but a potential disadvantage is the short duration of action.  There are several studies that promote the use of DDAVP, listed below:


Study design

Sample size and characteristics



Mannucci et al. (1983)19 Retrospective, double blind, placebo controlled Patients with chronic renal failure receiving hemodialysis with prior history of bleeding and bleeding time >10 min (n = 12) Patients with increased bleeding time undergoing surgery (n = 9) One dose (0.3 g/kg i.v.) DDAVP versus placebo One dose (0.3 g/kg i.v.) DDAVP Bleeding time normalized in 5 of 12 patients 1 h postinfusion, 2 of 12 patients 4 h postinfusion, and 1 of 12 patients 8 h postinfusion No excessive blood loss during surgery
Kohler et al. (1989)73,a Prospective, randomized, double blind, placebo controlled Patients receiving hemodialysis for indication of unknown etiology with bleeding time >15 min (n = 8) One dose (0.4 g/kg subcutaneous) DDAVP Bleeding time reduced in 7 of 8 patients and normalized in 2 of 8 patients Significant increase in concentration of von Willebrand factor
Watson and Keogh (1982)74 Prospective, single center Patients with chronic renal failure and bleeding time >12 min (n = 12; 4 receiving hemodialysis, 3 receiving peritoneal dialysis) One dose (0.4 g/kg i.v.) DDAVP Bleeding time normalized in 6 of 12 patients 1 h postinfusion, 3 of 12 patients 2 h postinfusion, but 0 of 5 patients 24 h postinfusion


all these are small (n=8-12) studies, but may be worth keeping desmopressin in your toolbox for bleeding renal failure patients. 

dose is 0.3-0.4 g/kg, IV/SQ, once.

Submitted by W. Brooks.

Reference(s): The use of desmopressin as a hemostatic agent: A concise review, Franchini, et. Al, American Journal of HematologyVolume 82, Issue 8, Article first published online: 9 MAY 2007;  Evidence-based treatment recommendations for uremic bleeding, Hedges, et al, Nature Clinical Practice Nephrology (2007) 3, 138-153; picture

The Acromioclavicular Separation: What do I need to know?

28 Jun

There are 6 types of AC separations that are treated differently:

Type I: AC ligament sprain w/ joint intact.  Treated w/ ice, rest, protection w/ sling.

Type II: AC ligament torn, coracoclavicular ligament intact, AC joint subluxed.  Treated with ice, analgesia, 3-7 days of immobilization in a sling.

Type III: AC and CC ligaments torn, complete dislocation of the jointMostly non-op.  Rest, ice, immobilization for 2-3 weeks.  Return to normal activity in 6-12 weeks.

Type IV: Complete dislocation w/ posterior displacement of the distal clavicle into or through the trapezius.  Needs reduction-open or closed followed by conservative treatment similar to Type III.

Type V: Superior dislocation of the jointof 1-3 times normal spacing, disruption of the deltotrapezius fascia.  Requires open reduction, reconstruction of the CC ligament, and repair of the deltotrapezial fascia.

Type VI: Complete dislocation w/ inferior displacement of the distal clavicle into a subacromial or subcoracoidposition.  Requires open reduction and can sometimes damage neurovascular bundle beneath.

Submitted by W. Brooks.

Reference(s): UpToDate, Decision making: operative versus nonoperative treatment of acromioclavicular joint injuries, Bradley JP, Elkousy H, Clin Sports Med. 2003;22(2):277.; picture

Ruptured Globe Management in the ED

27 Jun

Exam findings for open globe include:

  • obvious corneal/scleral laceration,
  • volume loss to eye,
  • uveal/iris/ciliary body prolapse,
  • eccentric pupil,
  • intraocular protruding foreign body.

Initial management of the open globe in the ED includes:

  • CT imaging with orbital cuts,
  • NPO,
  • do not remove foreign bodies,
  • avoiding eye manipulation as to avoid increasing intraocular pressure,
  • elevate HOB to 30 degrees,
  • treat nausea aggressively,
  • analgesia,
  • avoiding eye drops,
  • IV antibiotics,
  • definitive care by ophthalmology 

Submitted by W. Brooks.

Reference(s):; picture

The Hypoglycemia Pediatric Patient

26 Jun


Your next patient is a 6 yo girl who presents with altered mental status. Bedside glucose is 12. Now what?

Causes of hypoglycemia in pediatric patients:

The differential is broad, but can be categorized into these main groups:

  • Disorders of carbohydrate metabolism, including
    • Disorders of glycogenolysis
    • Disorders of gluconeogenesis
    • Galactossemia
    • Hereditary Fructose intolerance
  • Disorders of Amino Acid Metabolism
  • Disorders of Fatty Acid Metabolism
  • Increased utilization of Insulin
    • Hyperinsulinism
    • Ingestion of oral anti-hyperglycemics
    • Error in calculating insulin doses when patient is a Type I diabetic
  • Miscellaneous causes
    • Ketotic hypoglycemia
    • Hormone deficiencies
      • Growth Hormone deficienct
      • Cortisol deficiency
    • Ingestions
      • Alcohol
      • Salicylates
      • Beta-blockers
      • Oral anti-hyperglycemics
    • Surgery
    • Sepsis


Recognizing the hypoglycemia is the first step. Many of the causes of hypoglycemia will only be determined after a detailed inpatient workup.

Our job is to rule out the treatable causes such as ingestion and sepsis and treat accordingly.

These patients will often require D10 or D25 infusions to maintain euglycemia.

Under stress conditions, children with adrenal insufficiency should receive Hydrocortisone in the following doses (these doses will sustain appropriate levels for 6 hours)

  • ❤ years: 25 mg
  • 3-12 years: 50 mg
  • >12 years: 100 mg

Submitted by W. Brooks.

Reference(s): UpToDate; Donohoue PA. Adrenal disorders. In: Pediatric Practice Endocrinology, Kappy MS, Allen DB, Geffner ME. (Eds), McGraw Hill Medical, New York 2010. p.132-190.; picture

Lemierre’s syndrome

25 Jun

What is it?

Bacteremia secondary to infected thrombosis that occurred as a result of peritonsilar abscess.

How does it occur?

usually occurs in young, healthy patients who have a Strep infection that progresses to peritonsilar abscess without proper treatment.

Within the abscess, anaerobic bacteria (most common Fusobacterium necrophorum) grow.

The bacteria eventually penetrate into the neighboring jugular vein and cause a thrombus to form.

The thrombus can subsequently cause smaller clots to be scattered in the blood stream, leading to, among other consequences, septic emboli into the lungs.

How do I treat it?

The most difficult step in treating the disease is recognizing that the patient has the infection since it is so rare.

So, always keep this diagnosis in the back of your mind with someone who has a good story for a PE and is septic appearing and/or had a recent or concurrent oropharyngeal infection.

Start the patient on antibioticsF. necrophorum is generally susceptible to beta-lactams, flagyl, clindamycin, and 3rd generation cephalosporins. 

Submitted by W. Brooks.

Refernce(s): Wikipedia; Lemierre’s Syndrome, Wright, et al, Southern Medical Journal, May 2012; picture from NEJM

takotsubo cardiomyopathy

22 Jun


In postmenopausal woman, Takotsubo cardiomyopathy is a common cause of chest pain and ECG changes with elevated cardiac enzyme levels usually (but not always) following psychological or physiologic stress.  

Pathophysiology remains controversial. Unlike myocardial infarction, the prognosis is usually benign with full restoration of contractile functions



  • Transient left ventricular apical ballooning syndrome
  • Stress-induced cardiomyopathy (SICM)
  • Broken heart syndrome 
  • Ampulla cardiomyopathy. 

Defined as transient LV apical hypokinesia without significant coronary artery stenosis in angiography or cardiomyopathy.  

The mid-ventricle and apex of the heart, when viewed by echocardiogra

phy or catheterization, has a spherical bottle with narrow neck in time of heart systole which resembles the old Japanese octopus trap called “Takotsubo.” 

Most patients are postmenopausal women with typical or atypical angina referred after an intensive emotional or surgical stressor such as serious environmental stimulations, suddenly loss of one loved him/her, complicated medical diseases, and noncardiac surgery with ECG changes and elevation of cardiac biomarkers.  

Usually, coronary angiogram doesn’t show stenotic lesions.  

Initially, left ventricular ejection fraction is low; afterwards it recovers within one month.

Submitted by J. Gullo.

Reference(s): PMID: 22097239PMID: 22091255; picture; picture 2

What’s Pradaxa? Can I make people stop bleeding?

21 Jun


Mechanism of action of Pradaxa (dabigatran):

  • The drug itself is a pro-drug that is converted into an active metabolite in vivo
  • The active metabolite is a direct thrombin inhibitor that inhibits free and fibrin-bound thrombin
  • inhibits anticoagulation by preventing thrombin-mediated effects including cleavage of fibrin to fibrin monmomers, activation of V, VIII, XI, and XIII, and inhibition of thrombin-induced platelet aggregation.

Several potential antidotes have been studied for reversal:

  • Recombinant Factor VIIa
    • Had no effect on the prevention of excess hematoma expansion induced by dabigatran in one study
    • However, in a study using blood from healthy volunteers, rFVIIa successfully reversed the actions of dabigatran by reducing clot initiation time to baseline levels
  • Prothrombin Concentrate Complexes
    • In one study, PCC’s failed to reduced the effects of Pradaxa
    • PCC however was successful in reversing the effects of dabigatran in a model of intracerebral hemorrhage, where excess hematoma expansion was prevented
    • Overall, more research is needed to determine correct dosing of PCC’s to reverse Pradaxa.


When faced with a patient with serious or life-threatening bleeding who is on Pradaxa, rFVIIa and PCC’s seem to be the only potential treatments, though the data is not conclusive

Submitted by W. Brooks.

Reference(s): UpToDate; Reversal of Antithrombotic agents, Kenneth Bauer, American Journal of Hematology, Volume 87, Issue S1, p S119-S126, May 2012; picture