All posts by rabihgeha

VA morning report 3.19.18 Parkinsonism

Case summary

Thanks to Santo for presenting a case of a 73M who presented with “inability to walk” for months to years and multiple falls, and after an amazingly through exam by Santo was ultimately found to have Parkinson’s Disease.

Top pearls

1. The initial branch point in patients with a fall is to determine whether there was LOC [=syncope]. The causes of a  “mechanical” fall is usually multifactorial but may involve motor weakness [e.g., neuropathy], impaired sensory input [reduced proprioception, impaired vision etc], or gait apraxia [e.g, cerebellar dysfunction, basal ganglia diseases]. See below for an approach.

2. Idiopathic Parkinson’s disease lives within a spectrum of disorders = Parkinsonism. Other causes of Parkinsonism include drug-induced, vascular and lewy body dementia.

3.  Divide the symptoms of Parkinsons disease in into non-motor [e.g., constipation, REM sleep disorder] and motor [e.g., rigidity]. Most patients follow a standard evolution of non-motor and motor symptoms. See below.

An approach to falls




Evolution of symptoms of idiopathic Parkinson’s disease



VA morning report 3.5.18 – Syncope and cardiac amyloidosis

Case Summary

Thanks to Arvind for presenting a fascinating case of a 40M who presented with recurrent syncope and heart failure found to have cardiac AL amyloidosis!

Top pearls

1.  Vasovagal and idiopathic are the most common causes of syncope. History, physical exam, and EKG suffice for most patients. Reserve advanced testing [e.g. ziopatch, TTE] for patients with a positive initial evaluation.

2. A RBBB does not lead to right-axis deviation and thus an alternative cause for the axis deviation should be sought. In this patient, this was a LPFB.

3. Amyloidosis is a heterogenous group of disorders that result from the deposition of a misfolded protein.  The type of protein determines the deposition pattern and therefore the clinical manifestations. For example light chain amyloidosis –> heart, kidney, nerves > liver;  AA amyloidosis —> kidney > liver > heart.


Here’s one approach to syncope




VA ICU report – 3.2.18 abdominal compartment syndrome

Case summary

Thanks to the ICU team for presenting a case of a 53M w/ CHF and cirrhosis who developed a hematoma compressing the IVC after a paracentesis.

Top pearls

  1. The initial hemoglobin after a bleeding event does not reflect the true extent of blood loss. Time, usually hours, is needed to equilibrate with the plasma.
  2.  Gynecologic complications [e.g, ruptured ectopic] account for the majority of spontaneous hemoperitoneum. In a patients with cirrhosis, ruptured HCC, intra-abdominal varices and a splanchnic artery aneursym rupture are important considerations.
  3. Abdominal compartment syndrome is defined as sustained abdominal hypertension [>20mmHg] with evidence of end-organ damage – usually AKI and hypotension. More below.

Abdominal compartment syndrome



  • Normal abdominal pressure = 5-7
  • Intra-abdominal HTN is when pressure > 12
  • Grade1: 12-15;  G2 16-20; G3 21-25; G4 > 26

Abdominal compartment syndrome refers to sustained HTN, usually > 20 + evidence of organ dysfunction

How is the pressure measured?
Bladder pressure –  a good surrogate of abdominal pressure if done correctly
  • Patient is supine
  • Measured at end-expiration (lung inflation increases intra-abdominal pressure)
  • Wait 30-60s after instillation of warm saline (colder saline induces bladder contraction)
    *Obesity can influence baseline
Intra-gastric balloon measurement is an alternative way
  • Similar to abdominal distention, it is either an increase in
    • Gas
      • Ileus
    • Solid
      • Compressive mass on IVC
    • Liquid — most frequent cause
      • Massive ascites
      • Intraperitoneal hemorrhage
  • Also consider reduced pulmonary and abdominal wall compliance.
  • Intrabdominal hypertension —> impaired venous return –>
    • Acute kidney injury from renal vein compression
    • Hypotension from reduced pre-load
Pulmonary/Abdominal wall compliance
  • Vent synchrony
  • Pain control
  • Consider paralytics
  • Supine position
Gas decompression
  • NG +/- rectal decompression
  • Motility agents e.g., neostigmine
  • Paracentesis
  • Fluid restriiction
  • Diuresis
*Surgery as a last resort.

VA morning report 2.14 – Osteomyelitis

Case summary

Thanks to Sara and Renee for presenting a fascinating case of a 68F who presenting with weakness and found to have vertebral osteomyelitis, biopsy is pending.

Top pearls

  1. Patients with lower (thoracic, lumbar) vertebral disease (e.g., fracture, osteomyelitis) have a tough time sitting up due to the axial load this places on the spine.
  2. Vertebral tenderness to palpation is a highly insensitive sign for pathologic diseasesof the spine.
  3. The role of inflammatory markers (ESR, CRP) is for their negative predictive value in inflammatory/infectious/malignant causes of spinal disease (osteomyelitis, epidural abscess)
  4. Unlike osteomyelitis of the extremities, osteomyelitis of the spine is usually (1) hematogenous and (2) monomicrobial

Osteomyelitis Microbiology


VA morning report 2.12 – AKI and obstructive uropathy

Case Summary

Thanks to Scott for presenting a fascinating case of an 80M with well-controlled HIV and BPH who presented with AKI found to have bilateral hydronephrosis with resolution of his AKI with b/l nephrostomy tubes.

Top pearls

1. Obstructive uropathy is rare in young patients without LUTS. Consider deferring a renal ultrasound in the initial work up for AKI in these patients.

2. Both pre and post-renal causes of AKI have an abrupt response to treatment.  Response to treatment [e.g., IVF or nephrostomy tube placement] may occasionally be more informative than a detailed analysis of existing laboratory data [e.g., FeNa]

3. Most Dx tests of kidney injury are of the urine [UA, Uprotein/Cr, urine Na]. Especially in patients with concomitant anemia or thrombocytopenia, don’t forget a crucial blood test: the peripheral smear looking for schistoscytes.

Here’s one approach to AKI



VA morning report 2.2.17 – Candidemia!

Case summary

Thanks to our amazing ICU team for presenting the case of a 74M with chronic struvite stones who became hypotensive after stone retrieval found to have candidemia.

Top pearls

1. In an acute inflammatory state such as sepsis, the development of leukopenia is often  due to neutrophilic tissue migration. The thrombocytopenia that often develops in these cases may be to entrapment by NETs = neutrophil extracellular traps.

2. Like staph aureus – candida is the blood is never a contaminant.

3. Given the rise of azole-resistant candida, empiric therapy for candidemia is an echinocandin – see more below.

Candida Species



Approach to Candidemia


VA morning report – SVT and cardiac complications of radiation

Case Summary

Thanks so Sam for presenting an interesting case of a 75M s/p esophagectomy + chemo/rads for esophageal cancer who presented with chest pain and palpitations found to have atrial flutter with RVR.

Here’s one approach to supraventricular tachycardia


There are a variety of cardiac complications of radiation. 

Here’s an anatomic approach to these complications as well as recommendations about monitoring patients from a Cleveland Clinic review article.


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