All posts by rabihgeha

VA morning report 10.16.17: Another legionella case???

Case summary

Thanks to Hengameh and Max for presenting a very interesting case of a 66M with CLL, cutaneous eosinophilic syndrome who presented with dyspnea, cough and diarrhea found to have hyponatremia, hypophosphatemia and an elevated CK concerning for legionella!

Top pearls

1. Gerald Hsu taught use a lot about CLL. It is a disorder of  mature lymphocytes [CD 5 positive, smudge cells] and has a wide clinical spectrum ranging from an asymptomatic benign disease to an aggressive lymphoma with potential for transformation to a diffuse large B cell lymphoma.

2. In patients who truly have sudden onset of symptoms, consider [1] rupture of blood vessel/hollow viscus [2] Perforation of blood vessel/hollow viscus or [3] electrical [arrhythmia/seizure]

3. Legionella is a mutlisystem disorder that frequently causes pneumonia. High fever, relative bradycardia, CNS sx, GI sx, hyponatremia, hypophosphatemia and an elevated CK are also clues to the presence of legionella.

4. In a febrile patient, for each degree fahrenheit increase in temperature an increase of 10 beats/min in the HR is expected. Relative bradycardia refers to a less than expected pulse in a febrile patient. Beta-blockers are the most common cause. In the absence of these medications, infection by intracellular organisms [including Legionella!] or non-infectious fever are possible.


Here’s a short evernote about CLL.


Evernote about legionella:

Sudden onset of Symptoms

Sudden onset as reported by a patient does not always equal sudden in the way physician usually mean [e.g seconds]
Here is a great example of this phenomenon from a recent case report:
“A distinction must be made between sudden onset of visual loss and sudden discovery of preexisting visual loss. If the normal eye is inadvertently covered, a longstanding or gradual loss of vision in the other eye may be mistaken for acute loss”

Relative Bradycardia


  • Physiologically, for each degree fahrenheit increase in temperature, there should be a 10 beat/min increase in HR.
  • However, this only applies for temperatures >102F
  • Patients with conduction system disease or AV block blockade are excluded.

Official criteria + expected values




Note the propensity for intracellular organisms.




VA morning report 10.10: Pruritis and cholestasis!

Case Summary

Thanks to Diana Tobler for presenting an interesting case of a 60M with HFrEF and HCV who presents with pruritus found to have cholestasis likely from congestive hepatopathy superimposed on HCV cirrhosis.

Top pearls

  1. Pruritus is often due to a primary skin disorder. In patients without a primary rash, consider systemic causes [liver, renal, thyroid, and hematologic], neurologic disease [multiple sclerosis] and psychiatric diseases.
  2. Breakdown cholestatic liver disease into extrahepatic [disorder of the large caliber bile ducts] and intrahepatic [diseases of the bile ducts within the liver]. See below for one approach.
  3. Congestive hepatopathy results in a myriad of liver test abnormalities. Usually the bilirubin is < 3 and is mostly indirect.


Primary skin conditions account for the majority of cases. In these situations, studying the primary rash will help clarify the Dx.

*Caution: it is important to distinguish a primary skin rash from changes secondary to chronic scratching [e.g. prurigo nodularis]

Skin disorder with prominent pruritus
  • Atopic dermatitis – eczema
  • Contact dermatitis
  • Lichen Planus
  • Xerosis
  • Infections
    • Scabies
    • Lice
    • Bed bugs

Occasionally, pruritus may be due to a systemic condition. Here is one approach



Here’s one approach:


Congestive hepatopathy 

  • Most patients are usually asymptomatic and the diagnosis is entertained when patients have hepatic biochemical abnormalities.

Liver labs in congestive hepatopathy

There are no characteristic patterns of LFT changes in hepatic congestion. Some common abnormalities include

  • Elevated bilirubin
    • Usually < 3
    • Most indirect
  • Alkaline phosphatase
    • Mildly elevated
      • The mild elevation helps distinguish from the higher levels associated with biliary obstruction
  • Transmintiis
    • Usually less than 3 x the upper limit of normal.
  • INR
    • Usually <1.5

Acute right heart failure

Rarely, patients with acute right heart failure leading to hepatic congestion can have:

  • RUQ pain
  • Markedly elevated bilirubin [> 10]
  • AST/ALT > 500 if cardiogenic shock is present.






VA ICU report 9.29.17 – Tox Bundle and calcium channel blocker toxicity

Case summary

Thanks to the ICU team for presenting a great case of a 70M with depression who presented with after an overdose of clonidine and amlodipine c/b refractory shock now improved!

Top pearls

  1. In patients with a suspected toxidrome, it is important to try to establish:
    • What drug? immediate versus extended release
    • When was it taken?
    • How much?
    • Other exposures?
    • Interactions with other medications?
  2. Always think about ongoing exposures and needing “source control”
    • Skin exam [e.g fentanyl patch]
    • GI [swallowed pills]
  3.  Calcium channel blocker toxicity is fairly morbid. It causes 14% of drug-related cardiovascular toxicity but is associated with with 40% of the mortalities related to such drugs! See below for details.

Tox Bundle

Here’s one way to approach patients with a suspected toxidrome

Tox Bunle.png

After getting the above data, here’s one way to consider potential causes


Calcium Channel Blocker [CCB] toxicity 


  • CCB are divided into dihydropyridine [e.g amlodipine] and non-dihydropyridine [e .gverapamil]
    • Toxicity may be related to primary mechanism
      • Dihydropyridine —> vasodilation + reflex tachycardia
      • Non-dihydropyridine —> braycardia, reduced contractility
    • However, at high doses, dihydropyridines can blunt cardiac contractility and reduce the heart rate


  • CCB toxicity accounts for 15% of drugs causing cardiovascular toxicity
    • Morbid —> 40% of all deaths related to CV toxicity

Clinical presentation

  • Toxicity usually observed with >5x the baseline dose
  • Bradycardia + hypotension are the most common findings
  • Other features include
    • Hyperglycemia
      • Inhibition of calcium-mediated insulin release
    • Relative preservation of mental status despite low BP

*The above two features distinguish help distinguish CCB from beta blocker toxicity which can be accompanied by hypoglycemia and disproportionally reduced mental status compared to BP.


  • “Source control”
    • Activated charcoal
      • Most helpful if within 1-2h
      • Avoid in patients with high aspiration risk
    • Whole bowel lavage
      • Instillation of polyethylene glycol via NG lavage at around 2L/h with goal
      • Consider if extended release formulation
  • Targeted therapy for CCB

The evidence for the therapies below comes from case series and therefore is limited in quality. Often, a combination of these interventions is needed

  • IV calcium
    • Calcium chloride preferred over gluconate
      • Requires central line
    • Consider calcium infusion
    • Goal Ca of 12-13
  • Glucagon
  • Insulin + Dextrose
    • Higher body of evidence behind this intervention
    • Requires high doses of insulin
      • Aggressive manage glucose and K
  • Lipid infusion
    • Serves as a “sink” for the CCB
  • Pressors
    • Norepinephrine is first line.

VA Ambulatory report 9.27.17 – Anemia macrocytosis and MDS!

Case summary

Thanks to Vaibhav for presenting a case of an 88M with EtOH use disorder who presented with macrocytic anemia concerning for MDS complicated by acute on chronic anemia due to iron deficiency.

Top pearls

1. MCV is a very helpful clue in understanding the cause of anemia, but cannot be fully relied upon. Causes of macrocytic anemia can present with a normal MCV due to a concomitant normocytic or microcytic anemia [e.g. iron + b12 deficiency]

2. Theoretically, you can divide macrocytic anemia into megaloblastic versus non-megaloblastic to shorten the DDx (based on smear). Practically, it wise to initially consider common things in all patients: b12 deficiency, EtOH use, liver disease and drugs (hydroxyurea, methotrexate). See more below.

3. In patients with an established cause of anemia be sure to consider other causes  when they present with a worsening hemoglobin [e.g. GI bleed in patient with established MDS]


Here is one approach:

Anemia .png

  • As Vaibhav reminded us, in patients with an established cause of anemia be sure to consider other causes when they present with a worsening hemoglobin [e.g. GI bleed in patient with established MDS]

Macrocytic anemia

  • While the MCV is a very helpful clue in understanding the cause of anemia, it cannot be fully relied upon:
    • Causes of macrocytic anemia can present with a normal MCV due to a concomitant normocytic or microcytic anemia [e.g. iron + b12 deficiency]
  • MCV is still very helpful in guiding the initial work up:
    • You can divide macrocytic anemia into megaloblastic [cell is big because of problems with DNA —> hypersegmented PMN on smear]  versus non-megaloblastic [cell is big due to other reasons] to shorten the DDx + help remember these causes (see below).
    • Practically, it wise to initially consider [and test/assess for] common things in all patients: b12 deficiency, EtOH use, liver disease and drugs (hydroxyurea, methotrexate).

Macrocytic Anemia


Check out this awesome blog post from Anna Parks!


VA morning report 9.12.17 – Altered mental status, PVR negative retention and infection treatment “failure”

Case Summary

Thanks to Adam Tabbaa for presenting an interesting case of a 70M with spinocerebellar ataxia who presented with AMS concerning for a UTI c/b persistent leukocytosis found to have urinary obstruction from constipation!

Top pearls

1. Altered mental status has a broad DDX [see below for one approach]. Before diagnostics return, consider rapidly assessing for: [1] need for airway protection [2] signs of ICP [3] Finger stick –> thiamine + glucose [4] evidence of opiate overdose. These conditions can be addressed rapidly without further diagnostics.

2. We rely on the bedside ultrasound [= PVR] to help diagnose urinary retention. The measurement can be inherently misleading [e.g ascites misread as urine in the bladder] and there are cause of PVR negative obstruction.

3. Consider the natural history of an infection before undergoing a work up for treatment “failure” [see below for one approach]. For example, fever is common in uncomplicated pyelonephritis for up to 72 hours.

Altered mental status

Here is one approach to altered mental status. Remember to rapidly consider

[1] Airway protection –> ?intubate

[2] Signs of elevated ICP —> ? intubate/mannitol/3% NS/Neurosurgery consult

[3] Fingerstick glucose –> D50 + thiamine

[4] Evidence of opiate overdose —> Nalaxone


The  toxin category can be tricky. Here is one way of breaking it down –


Urinary obstruction

We often rely on the bedside bladder ultrasound or post void residual [PVR] to rapidly diagnose urinary obstruction.

False positive bladder ultrasound 

False positives occur when something else fools the scanner. This can include

  • Adipose tissue
  • Ascites

*Pearl from Colin Purmal – use the ultrasound probe to visualize the bladder when suspicious of a false positive.

False negative

Bilateral ureteral obstruction or external compression of the bladder can cause obstruction with low volume in the bladder

  • Bowel
    • Constipation
    • Large bowel obstruction
  • Pelvic malignancy
    • Ovarian carcinoma
  • Retroperitoneal hematoma
  • Retroperitoneal fibrosis

*Really, any diffuse retroperitoneal process

Infection treatment “failure”

  • Infections have a naturally history that must be taken account before invoking failure of therapy. For example –
    • fever is normal up to 72 hours in patients with uncomplicated CAP and pyelonephritis
    • patients with PCP often get worse before they getter better
  • Here is one approach to consider when thinking about this problem

Infection Rx failure .png




VA morning report – 9.11.17: CLL and autoimmune hemolytic anemia

Case Summary

Thanks to Andrew for presenting a case of an elderly man with CLL who presented with falls and anemia and was found to have autoimmune hemolytic anemia!

Top pearls

1. Acute anemia is almost always due to [1] blood loss or [2] hemolysis, rarely aggressive bone marrow diseases [e.g AML] can cause anemia of rapid onset.

2. Immune hemolytic anemia and microangiopathic hemolysis are the two most common causes of hemolysis. If difficult cases, consider using an anatomic approach. See below.

3. Chronic lymphocytic leukemia is the most common leukemia in adults and is usually diagnosed in asymptomatic patients getting a CBC for other reasons. See below for a detailed illness script on CLL.

Acute Anemia

  • Anemia has a broad DDx. Acute anemia, however, is usually due to:
    • Blood loss
      • GI tract
      • Cutaneous
      • Retroperitonal
      • Extremity
      • Pleural space
      • Lungs
    • Hemolysis
    • rarely, aggressive bone marrow diseases [e.g AML] can cause anemia of rapid onset.

Hemolytic anemia

  • The smear can provide important information on the causes hemolysis.
  • Two common causes include microangiopathic hemolytic anemia [schistocytes] and immune hemolytic anemia [spherocytes in most cases]

Here is one anatomic approach to hemolytic anemia –



Immune hemolytic anemia is further divided into

  • Autoimmune: antibdoy to self RBCs.
    • Idiopathic: 50%
    • Secondary to:
      • Autoimmune disorder
      • Infection
      • Malignancy
  • Alloimmune = exposure to outside RBCs induces hemolysis and only non-native RBCs are destroyed. Self RBCs are usually spared.
    • Transfusion
  • Drug-induced

Autoimmune hemolytic anemia is further broken down into

Warm autoimmune hemolytic anemia

  • IgG antibody that induces extravascular hemolysis
  • Majority are idiopathic (50%)  but some precipitants (in order of frequency) include
    • Lymphoproliferative disease
      • CLL
    1. Autoimmune disease
      • SLE
    2. Infections
      • HIV/EBV
    3. Malignancy – typically liquid
      • Lymphoma
  • Treatment:
    • Watchful waiting if hemolysis is not severe
    • Steroids —> IVIG —> Ritixumab —> Splenectomy
      • Steroids need days to work
      • Effect of IVIG is more rapid
Cold autoimmune hemolytic anemia (1/3 of cases)
  •      IgM typically attaches in the periphery [colder environment] and detaches in the warmer core, leaving complement behind –> C3b on coombs testing
  • Majority are idiopathic [50%], but secondary causes include
    • Lymphoproliferative – 50%
      • Waldenstorms
    • Infection – 30%
      • Mycoplasma
    • Malignancy
      • Solid > liquid
  • Treatment
    • Avoidance of cold is most important
    • Treat the underlying cause
    • IVIG/Plasmapharesis/Rituximab/Chemo


Here is an illness script for CLL: