All posts by rabihgeha

VA ICU report 6.23.17: Burns and shock!

Case summary

Thanks to Vijay and the ICU team for presenting a great case of a 68M w/ diabetic neuropathy who presented with thermal burns to the legs c/b by likely septic shock.

Top pearls.

  • Superficial skin conditions (e.g. cellulitis) rarely lead to hemodynamic comprise. The presence of systemic illness should prompt consideration for a deeper space process (e.g necrotizing fasciitis).
  • For patients with burns:
  1. Calculate the affected BSA and assess depth of skin involvement
  2. Use the Parkland Formula for fluid repletion
  3. Contact surgery early
  4. Consider transfer to a burn center
  • On initial assessment, four categories of shock (distributive, hypovolemic, cardiogenic and obstructive) can be sorted by SVR (cold skin –> high SVR; warm skin –> low SVR) and JVP.


Assessing the extent of skin involvement (body surface area and depth) is the an important initial step

  • Use the rule of 9’s to estimate BSA involved
    • 9%: head + neck, upper extremity
    • 18%: lower extremity, torso, back
  • Estimate the depth of involvement Burns.png


  1. Consult surgery early
    • Early debridement (< 1 week) reduces risk of super-infection
    • Early consideration of escharotomy reduces risk of compartment syndrome from the edema that naturally follows a burn injury.
  2. Use the Parkland formula to calculate fluid requirements
  3. Consider transfer to a burn center. Some criteria include (full list on UpTodate):
    • Full thickness burn on BSA > 10%
    • Involvement of the face, hands, feet, genitals or joints
    • Third degree burns


Determining the etiology of shock is critical for management.  This is often made easier when data from invasive monitoring is available (SvO2, CVP etc).

On the initial assessmentgauging the SVR (warm skin –> low SVR; cool –> high SVR) and the JVP provide strong clues to etiology of shock.

Shock INitial.png

Shock Approach.png




VA Report 6.20: Leukocytosis and Cecal mass

Case Summary

Thanks to Kendra Wulczyn for presenting an amazing case of a 68M w/ COPD who was found down, and found to have a leukocytosis and a cecal mass ultimately diagnosed with diffuse large B-cell lymphoma.

Top pearls 

1. C.diff PCR cannot distinguish between colonization and infection. Approximately 10% of the population is estimated be colonized with C.diff

2.  Neutrophilic leukocytosis usually represents infection. Other causes of polyclonal neutrophilia include drugs, autoimmune disease, and malignancy. Rarely, monoclonal neutrophilia occurs from myeloproliferative diseases.

3. The differential diagnosis of a cecal mass is extensive. Carefully consider structures adjacent to the cecum that may mimic a cecal mass (psoas abscess, tubo-ovarian abscess)

Neutrophilic Leukocytosis

The vast majority of neutrophilic leukocytosis is infection. If an extensive search for infection is negative, consider the following list of non-infectious causes of neutrophilic leukocytosis.

*While you diligently rule out infection, the smear can provide clues to a non-infectious cause (e.g basophilia/eosinophilia may suggest myeloproliferative disease).


Lymphocytic Leukocytosis

Rarely, the leukocytosis will be predominantly lymphocytic:


Cecal Thickening

The differential diagnosis of cecal thickening is extensive, partly because of variety of structures adjacent to the cecum : ileum, lymph nodes, and appendix.

Before proceeding down the cecal thickening pathway, consider (and talk to your radiologist) processes adjacent to the cecum that can mimic a cecal mass (psoas abscess, tubo-ovarian abscess)



VA ICU report 6.16.17: Hypernatremia

Case summary

47M with mutism p/w AMS, profound weight loss and found to have marked hypernatremia

Take aways

  1. Approach to hypernatremia
    1. Consider free water loss (renal, GI, insensible loss)
    2. Reduced access to free water (dementia)
    3. Hypertonic intake (3% NS, ocean water)
  2. Diabetes insipidus implies impaired urinary water reabsorption and therefore urine osms are inappropriately lower than serum osms.
  3. Treatment
    1. Determine acute versus chronic
    2. Calculate free water detect
      1. If acute correct over 24 hours
      2. If chronic correct 10mEq/day
    3. Reassess frequently


Approach to hypernatremia




The principles of treatment in hypernatremia are similar to those in hyponatremia and therefore it also important to determine:

  • Acute (< 24 hours) versus chronic (> 24 hours)
    • Acute: correct over 24 hours
    • Chronic: correct by 10mEq/24 hours
      • Why? With aggressive repletion of free water, there is a risk of cerebral edema. This risk is less than that of aggressive correction of hyponatremia (–> osmotic demyelination syndrome) but is more likely in patients with higher initial Na
  • Symptomatic versus asymptomatic

Details of correction of chronic hypernatremia 

  • Step 1: use the (1) patients’ weight (2) current sodium and (3) goal sodium (usually 10mEq less than current sodium) to calculate the free water deficit for the day.
  • Step 2: divide the free water deficit/24 hours and infuse D5 H20 at that rate
  • Frequently recheck your Na and adjust your rate by starting back at step 1

*Consider making the patient NPO to ensure accuracy of free H20 intake (especially initially).

*In patients with DI, their free water clearance via the kidneys may be dynamic. Therefore, monitoring the urine osm (along with renal or endocrine) is important.

Concomitant hypovolemia

  • For patients with concomitant hypovolemia obtain second PIV (if possible) and bolus PRN (e.g. soft blood pressures)
    • Separating the treatment of hypovolemia from addressing your free water deficit will help  maintain better control of your sodium correction.


VA report 6.12.17: HACEK endocarditis

Case Summary
Thanks to Ashley Stein-Merlob for presenting a fascinating case of a 59M with HFrEF s/p ICD/CRRT p/w fatigue and chills found to have Aggregatibacter bacteremia concerning for infective endocarditis.

Top pearls

  1. In approaching a patient with bacteremia, consider
    • Source of infection (skin, oral flora, GI, GU)
    • Metastatic foci of infection
      • Endocarditis
      • Osteoarticular (osteomyelitis, septic arthritis)
      • Visceral abscess (spleen, liver, kidney)
      • CNS (abscess, mycotic aneursym)
  2. Further divide endocarditis into
    • Acute (staph aureus) versus subacute (other organisms)
    • Native valve versus prosthetic (valve or leads)
  3. Subacute bacterial endocarditis is characterized predominantly by immunologic phenomena
    • Positive rheumatoid factor
    • Glomerulonephritis
    • Splenomegaly, lymphadenopathy
    • Inflammatory back pain.

Infective Endocarditis

To characterize the disease process, endocarditis is further broken down into

  • Acute vs subacute 
    • Acute infective endocarditis is most often caused by Staph aureus, which has the ability to infect undamaged, native valves and presents more abruptly (days).
    • Subacute bacterial endocarditis is caused by less virulent organisms (e.g. strep viridans species) is more likely to involve damaged valves (or prosthetic valves) and  presents subacutely (weeks) with more immunologic phenomenon (see above).
  • Native versus prosthetic valve
    • This distinction influences the microbiology (more coag. negative staph in prosthetic valve disease) and treatment (early surgical intervention in prosthetic valve endocarditis)

Here is a breakdown of the causes of endocarditis:


HACEK organisms

The HACEK organisms have been recently renamed and now include

  • Haemophilus species
  • Aggregatibacter species
  • Cardiobacterium hominis
  • Eikenella corrodens
  • Kingella kingae

These organisms are indigenous flora that colonize the orophaynx and likely play a role in oral infection. They are an infrequent cause of endocarditis (~4%).

Historically, considered as causes of “culture-negative” endocarditis, these organisms are now more easily cultured.

Features of HACEK endocarditis compared to non-HACEK endocarditis:

  • Younger patients (mean 47 vs 61)
  • High prevalence of immunologic manifestations (30% vs 20%)
  • High prevalence of stroke (25% vs 17%)
  • Lower prevalence of CHF (15% vs 30%)
  • Lower in-hospital mortality (4% vs 18%)

More about Aggregatibacter species

  • Accounts for 35% of HACEK infections
  • A positive blood culture represents true bacteremia in 100% of cases
  • File this in your mind as an “abscess-forming organism” which is has propensity for endocarditis, but also causes
    • Periodontal abscess
    • Septic arthritis
    • Osteomyelitis
    • CNS abscess
    • Thyroid abscess


VA Morning Report 6.6.17: Ascites, transaminitis and decompensated cirrhosis

Scott Bauer presented a great case of a 51M with EtOH use disorder who presented with subacute abdominal pain, distention and jaundice initially concerning for alcoholic hepatitis, ultimately found to have decompensated alcoholic cirrhosis.

1. Distinguishing ascites from other causes of abdominal distention is challenging. Consider supplementing your physical exam with bedside ultrasound.
2. The ratios of liver enzymes can provide strong clues about the etiology of liver injury – AST/ALT > 2 is highly suggestive of alcohol-related liver disease.
3.  Patients with cirrhosis are at risk of decompensation from a wide variety of factors including:
  • Vascular injury (portal vein thrombosis)
  • Infection (viral hepatitis, SBP, PNA, UTI)
  • Malignancy (HCC)
  • GI bleeding
  • Toxins/Meds (alcohol, acetaminophen, NSAIDs, diuretics)

The cause of abdominal distention can categorized into
  1. Solid
    • Hepatomegaly
    • Splenomegaly
    • Adiposity
    • Malignancy
  2. Liquid
    • Ascites
  3. Gas
    • Bowel obstruction/ileus

Several physical exam maneuvers can help distinguish these causes (e.g careful palpation for organomegaly, assessment for tympany, and fluid wave).

A bedside ultrasound is a great addition to this tool box.

Here is one approach (anatomic) to the DDx of transaminitis
The ratio of liver enzymes can also inform the DDx.
  • Extra-hepatic AST
    • Rhabdo
    • Hemolysis
    • Massive MI
  • Toxin-induced disease
    • Alcohol
    • Amiodarone
    • Vitamin A
Alk Phos/Tbili <4
  • Wilsons
  • ALT/LDH < 1.5 suggests ischemic hepatopathy
  • ALT/LDH > 1.5 suggests tylenol or viral hepatitis.

Decompensation refers to (1) worsening synthetic function (hepatic encephalopathy, hypoglycemia, coagulopathy) or (2) increased portal hypertension (increased ascites, variceal bleeding, hepatorenal syndrome) in a patient with cirrhosis.
While progression of the underlying disease is a common cause of decompensation, carefully assess for these possibilities:
  • Vascular injury (portal vein thrombosis)
  • Infection (viral hepatitis, SBP, pneumonia, UTI)
  • Malignancy (HCC)
  • GI bleeding
  • Toxins/Meds (alcohol, acetaminophen, NSAIDs, diuretics)

VA ICU report 6.2.17: Approach to abdominal pain + Sigmoid volvulus

Case Summary
Vijay presented an great case of an 84M with Afib and severe AS who presented with acute abdominal pain and found to have sigmoid volvulus treated with endoscopic decompression.

Top Pearls
1. Acute abdominal pain can be approached as:
  • Surgical causes (e.g perforation, mesenteric ischemia, volvulus) versus
  • Non-surgical causes

2. The history and physical exam are great tools to make diagnosis in abdominal pain but are less reliable if:

  • Older age (> 50)
  • Immunsuppression (e.g prednisone can easily mask intra-abdominal catastrophes)
  • Neurologic disease (e.g non-specific spasm can herald severe disease in patients with spinal cord disease)

3. KUB has limited sensitivity in detecting free air; increase yield with:

  • Upright KUB
  • Left lateral decubitus position (air seen better above liver)

Abdominal Pain
When considering causes of abdominal pain, it will be important to consider:
Thoracic causes
  1. Lower lobe pneumonia
  2. Acute coronary syndrome
Pelvic Causes
  1. Ovarian/testicular torsion
  2. Pelvic inflammatory disease
Abdominal Causes
We traditionally approach abdominal pain by quadrant (
This approach is less accurate in these patient populations:
  1. Older patients (> 50)
  2. Immunsuppression (e.g prednisone can easily mask intra-abdominal catastrophes)
  3. Neurologic disease (e.g non-specific spasm can herald severe disease in patients with spinal cord disease)
Think of surgical causes of abdominal pain early:
  • Bowel
    • Perforation
    • Obstruction
      • Large bowel obstruction more likely to require surgery than small bowel disease.
  • Vascular
    • Mesenteric ischemia
    • Abdominal Aortic Aneurysm rupture

Volvulus refers to torsion of a segment of the bowel. In adults, most common sites of volvulus are:
  • Sigmoid
  • Cecum
  • Other
    • Stomach, Gallbladder, Small Bowel etc
  • Colonic dysmotility predisposes the bowel to torsion
    • The obstruction develops slowly over days and accounts for the indolent presentation
  • The sigmoid colon is particularly vulnerable because chronic constipation —> elongation and dilation.
  • Volvulus is a rare diagnosis is adults and accounts for <10% of cases of large bowel obstruction.
  • Risk factors
    • Older age  (mean age 70)
    • Chronic constipation, recurrent obstipation or laxative dependence observed in 45% of patients undergoing surgery for sigmoid volvulus.
Clinical Presentation
  • Indolent presentation (85% of patients)
    • Progressive abdominal pain (with intermittent colicky pain) over days
    • Vomiting occurs several days after the pain
    • Obstipation is common but not universal (may have stool distal to volvulus and thus BMs and flatus)
  • Hyperacute presentation (15% of patients)
    • Sudden onset abdominal pain and obstipation —> higher risk for perforation
  • KUB – provides an initial clue
    • U-shaped distention which extends from the pelvis to the RUQ
  • CT – the diagnostic test of choice
  • Early GI and Surgery consults
  • Endoscopic decompression via sigmoidoscopy
    • Reduces the volvulus in up to 95% of cases
    • Role is as a bridge to surgery (converts an emergency procedure into a semi-urgent one)
  • Surgery
    • Surgical resection is usually performed within 72H
    • The goal is to prevent recurrence which occurs in up to 60% of patients.