It’s Anemia’s Brand

 Special thanks to Vishy for passing along this clinical pearl for the differential for anemia!


Iron deficiency anemia
Thalassemia – defective globin chain production
Sideroblastic anemia – hereditary, acquired (Etoh, INH, lead)

Anemia of chronic disease
Nephrogenic (decreased EPO)
Myleophthisis (marrow infiltration)
IV fluids – dilutional
Aplastic anemia – primary or drug induced
Sickle cell anemia

B12 deficiency
Reticulocytosis – compensatory from hemolysis
Nutritional deficiency of folate
Drugs (DNA synthesis inhibitors, dihydrofolate reductase inhibitors)

Clinical Pearls – Toxins and Antidotes







Beta blockers





Digoxin immune Fab

Ethylene glycol/methanol









Sodium bicarbonate

Tricyclic antidepressants

Sodium bicarbonate

Amniotic Fluid Embolism

Today at morning report with Dr. Vadia, we briefly touched on the topic of amniotic fluid embolism; this is an uncommon disorder that can have catastrophic consequences if  not recognized early.


  • Mortality rate used to be 86% –> 15% with ICU care
  • May be more common in older,multiparous women who experience prolonged, difficult labor

Clinical features

  • Usually occurs during childbirth, but has been described during pregnancy
  • Classic presentation: dyspnea, cyanosis, arrhythmia, hypotension, hemorrhage, disseminated intravascular coagulation –> cardiovascular collapse; however, presentation may be more subtle.
  • Maternal collapse usually occurs before fetal collapse, but vice-versa can occur and should trigger investigation into this diagnosis

Differential Diagnosis:

  • Obstetrical causes: placental abruption, uterine rupture, uterine atony, eclampsia, and peripartum cardiomyopathy.
  • Anesthetic causes include high spinal anesthesia and local anesthetic toxicity.
  • Nonobstetrical causes include pulmonary embolism, air embolism, anaphylaxis, septic shock, massive aspiration, transfusion reaction, and myocardial infarction.


  • Clinical diagnosis!
  • Amniotic fluid embolism may be an anaphylaxis-like reaction.
  • Serum tryptase levels are typically elevated and complement levels are usually low.


  • First resuscitate the patient!
    • arterial and a central venous catheter placement
    • supplemental O2
    • IV fluids and vasopressors if needed
  • Then, proceed to C-section.
  • Can also consider (all described in case reports only):
    • Uterine artery embolization
    • Plasma exchange
    • CVVHD
    • Inhaled nitric oxide
    • Circulatory assist devices: LVAD/RVAD, intraaortic balloon pump counterpulsation, and extracorporeal membrane oxygenation (ECMO).
    • Recombinant human factor VIIa in dire cases of DIC; has been associated with thrombotic morbidity and mortality (eg, stroke and pulmonary embolism).


  1. Gist RS, Stafford IP, Leibowitz AB, Beilin Y. Amniotic fluid embolism. Anesth Analg 2009; 108:1599.
  2. Tuffnell DJ. United kingdom amniotic fluid embolism register. BJOG 2005; 112:1625.
  3. Davies S. Amniotic fluid embolus: a review of the literature. Can J Anaesth. 2001; 48:88-98. 

Pre-medication prior to transfusion: what is the evidence?


Example Case: AB is a 60 year old male with a history HLD, HTN, and diverticulosis (recently diagnosed on colonoscopy last week) presenting with dizziness. His exam reveals orthostatic hypotension and sinus tachycardia, along with pale mucous membranes and hemoccult positive stool. Labs reveal a hgb of 6.3. After appropriate type and screen, a blood transfusion is ordered for the patient. The nurse notices that neither Benadryl nor Tylenol were ordered to be given prior to the transfusion. You, as the bright new intern, are asked to place the order. However, you then ask why these medications should be given prior to transfusion. Does this practice work to prevent allergic reactions or the febrile non-hemolytic transfusion reaction (fever, chills, rigors and hives)?

The cause for these reactions are likely multifactorial; they are thought to be the result of cytokine release or recipient antibodies directed against donor leukocytes or HLA antigens. The results of two RCTs have not proven the effectiveness of diphenhydramine or acetaminophen in preventing febrile non-hemolytic transfusion reactions (1, 2). This seems to agree with data from several previous non-randomized trial(3). Geiger et al. reviewed the available data and concluded that there is a “low reaction rates reported at many institutions even when premedication is not prescribed(4).”  A Cochrane review of the literature suggests that “current evidence from three trials in which 462 patients were analysed indicates pre-transfusion medication in any regimen does not reduce the risk of allergic and febrile non-haemolytic transfusion reactions(5).”  Take a look at the evidence below and decide for yourself – does your patient need pre-medication?

1. Wang SE, Lara Jr PN, Lee-Ow A, et al. Acetaminophen and diphenhydramine as premedication for platelet transfusions: a prospective randomized double-blind placebo-controlled trial.Am J Hematol 2002;70:191-194.
2. Kennedy LA, Case LD, Hurd DD, Cruz JM, and Pomper GJ. A prospective, randomized, double-blind controlled trial of acetaminophen and diphenhydramine pretransfusion medication versus placebo for the prevention of transfusion reactions. Transfusion 2008; 48:2285-2291.
3. Patterson BJ, Freedman J, Blanchette V, et al. Effect of premedication guidelines and leukoreduction on the rate of febrile nonhaemolytic platelet transfusion reactions. Transfusion Med 2000; 10:199-206.
4.Geiger TL and Howard SC. Acetaminophen and diphenhydramine premedication for allergic and febrile nonhemolytic transfusion reactions: good prophylaxis or bad practice? Transfusion Medicine Reviews 2007;21:1-12.4.  
5. Martí-Carvajal AJ, Solà I, González L, Leon de Gonzalez G, Rodriguez-Malagon N. Pharmacological interventions for the prevention of allergic and febrile non-haemolytic transfusion reactions. Cochrane Database of Systematic Reviews 2010. 



An Aspirin a day keeps the doctor away?

We all know of the cardiovascular benefits of aspirin — we start 81mg on nearly all patients with coronary artery disease, diabetes, acute coronary syndrome, etc. It results in significant risk reduction in re-infarction and mortality. But what else can this wonder-drug do? According to a new study in the Annals of Oncology, “prophylactic aspirin use for a minimum of 5 years at doses between 75 and 325 mg/day appears to have favourable benefit–harm profile; longer use is likely to have greater benefits.” Bold statement – read the article and decide for yourself (click the image below to be redirected to the article).



Guidelines Update

During several excellent discussions this week at morning report, from the the merits of cancer screening to elusive tropical diseases, we have covered what seems the be the entire gamut. Time to bring it back with some salient guidelines updates. Remember, these are important, evidence-based recommendations for the best practice of medicine – but they can only be effective when taken in the right context.


HIV Screening Guidelines: ELISA and Western blot? Not anymore. The CDC just released new guidelines for HIV testing, including completely new laboratory methods. The algorithm is below (click on the image to access the guidelines).

HIV guidelines


Lung Cancer Screening Guidelines: constant source of controversy, especially since the recent NLST data. Take a look at the Fleischner Criteria for following pulmonary nodules based on their relative malignant risk. Take a look at the USPSTF position statement.



AHA Pre-operative Cardiovascular Evaluation guidelines: Perioperative cardiac testing is discussed, including exercise and functional capacity, and includes a treatment algorithm for a stepwise approach to perioperative cardiac assessment. Recommendations for supplemental perioperative evaluation are also included. Just published last week!

Screen Shot 2014-08-07 at 11.02.34 PM


Hepatic encephalopathy: just published last month – the position statement from the AASLD helps guide diagnosis and management of this frequently encountered and enigmatic disease. Screen Shot 2014-08-07 at 11.07.44 PM


Chronic Kidney Disease: By popular demand, I have also added the KDIGO CKD guidelines introduced by Dr. Lu at grand rounds.


If you ever need to find the most recent guidelines (on anything, really) check out


Diarrhea, Confusion, Ataxia, Leukocytosis: Lithium Toxicity?

Today at VA Morning Report we had a great discussion about lithium toxicity. Below are some references that provide a nice summary. Key points:

  • Lithium has a narrow therapeutic level. It is thought that majority of patients on lithium have a history of supratherapeutic levels at some point during treatment.
  • Highest intracellular concentrations of lithium are thought to be in the brain and kidneys.
  • Serum levels do not correlate with severity of toxicity.
  • Certain medications such as diuretics, ACE inhibitors, and NSAID’s can precipitate renal failure with lithium use.
  • Signs and symptoms seen in lithium poisoning:
    • CNS: lethargy, confusion, seizures, coma, cerebellar dysfunction, tremor
    • GI: nausea, vomiting, diarrhea
    • Cardiovascular: sinus and AV node dysfunction (bradycardia, heart blocks, junctional rhythm), T wave inversions on ECG, hypotension
    • Hematological: leukocytosis (increased neutrophil and eosinophil counts)
    • Renal: polyuria (diabetes insipidus), renal failure, electrolyte disorders secondary to renal injury
    • Endocrine: hypothyroidism, myxdema coma, transient hyperglycemia, hyperparathryoidism
  • Management:
    • Assess airway
    • Consider GI decontamination if less than 2-4 hours (ie ipecac syrup) but avoid if patient has CNS dysfunction
    • Fluid resuscitation and electrolyte correction, avoid diuretics
    • Consider hemodialysis if renal function is compromised and severe or worsening neurological status. Recovery may be slow despite dialysis, due to compartmentalization of lithium in brain tissue.

Acute infectious diarrhea

Yesterday at VA Morning Report, we discussed about infectious diarrhea with Dr. Bedimo. Below are some key points from the discussion.

  • Diarrhea is considered acute if the duration is less than 14 days.
  • Etiology can be divided into two groups: inflammatory versus non-inflammatory.
  • Inflammatory organisms include Campylobacter, Shigella, Salmonella, C. diff, E. coli. Noninflammatory bugs include Noravirus, Rotavirus, S. aureus, B. cereus, C. perfringens.
  • Majority of acute infectious diarrhea cases are due to viruses.
  • Further diagnostic evaluation is warranted in patients who present with severe illness (fever, bloody diarrhea, hypovolemia, >6 bowel movements per 24 hours, immunocompromised).
  • Obtaining history of food consumption is important as some organisms present at certain hours after ingestion.
    • Symptoms that begin within 6 hours can be caused by release of toxin from S. aureus or B. cereus.
    • Symptoms that begin 8-16 hours after ingestion suggests C. perfringens.
    • At more than 16 hours from ingestion, consider both viral and bacterial infections.
  • Stool cultures and fecal ova and parasite tests are not required for every patient who presents with diarrhea. Consider these tests in patients who are immunocompromised, present with severe inflammatory diarrhea, have underlying inflammatory bowel disease, co-morbidities that put them at risk for complications.
  • Consider empiric antibiotics in patients who are immunocompromised, severely volume depleted, >1 week of symptoms, blood and pus in stools while awaiting culture results.

Check out this review article from The New England Journal of Medicine,  “Acute Infectious Diarrhea in an Immunocompetent Adults”:

UTSW Internal Medicine

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