All posts by rabihgeha

VA morning 5.29 – mixed acidosis and alkalosis

Case summary

Thanks to Peter Moore for presenting a fascinating case of a 74M who presented with leg spasms and found to have mixed primary respiratory alkalosis and lactate acidosis.

Approaches to respiratory alkalosis and lactic acidosis below!

Respiratory Alkalosis


Lactic acidosis



VA morning report – autoimmune hemolytic anemia

Case summary

Thanks to Jake from presenting the case of a 92M who presenting with dyspnea found to have warm autoimmune hemolytic anemia!

Top pearls

1. There are numerous causes of hemolytic anemia. One way to categorize them is by disease in the RBC environment [e.g., MAHA], on the RBC membrane [autoimmune hemolytic anemia] and within the RBC [e.g. G6PD] deficiency – see below for details.

2. The peripheral smear is highly informative in the work up of hemolysis. Specifically, the positive predictive value of certain findings [e.g., schistocytes] is often diagnostic. However, some findings have a poor negative predictive value.  For example, the absence of spherocytes does not exclude autoimmune hemolytic anemia [present in only  50%].

3. 50% of warm autoimmune hemolytic anemia is idiopathic. Secondary causes include certain malignancies [usually liquid], autoimmune disorders [e.g, SLE], infections [HIV] and drugs [Abx]



Warm autoimmune hemolytic anemia
  • Coombs test: IgG antibody —> extravascular hemolysis by splenic macrophages
  • Idiopathic – 50%
  • Secondary – 50%; in order of frequency
    • Lymphoproliferative disease
      • e.g. CLL
    • Autoimmune disease
      • e.g SLE
    • Infections
      • e.g, HIV
    • Immunodeficinecy
      • e.g, CVID
    • Drugs
      • e.g, ABX
  • DAT – antiIgG and evidence of hemolytic anemia


Work up
  • History + med-rec
  • Physical exam – lymphadenopathy, splenomegaly
  • Blood work
    • SPEP, immunoglobulins
    • ANA
    • Peripheral smear
  • Imaging
    • CT A/P > Ultrasound
  • Watchful waiting if hemolysis is not severe
  • Steroids —> IVIG —> Ritixumab —> Splenectomy
    • Recall that steroids need days to work
    • Effect of IVIG is more rapid
    • Low dose rituximab increasingly used
  • Varies according to underlying etiology
  • Overall
    • Cure – 50%
    • Partial remission = low dose steroid – 20%
    • Active disease – 30%

VA morning report – 4.24 – GCA and eGPA!

Case summary

Thanks to Paul for presenting a fascinating case of a 57F who presented with headache and blurry vision and was diagnosed with GCA despite a negative biopsy. After tapering steroids she developed eosinophilia, asthma, sinusitis and neuropathy and was diagnosed with eGPA!

Top pearls

  1. Giant cell arteritis is highly unusual in patients < 60!
  2. Giant cells Arteritis = GCA is  not the only vasculitis than can affect the temporal arteries. Rarely ANCA-associated vasculitides can lead to a non-GCA temporal arteritis
  3. eGPA is a disorder that develops over decades with an initial atopic phase [asthma, eczema], followed by a eosinophilic tissue phase [GI, pulm, cardiac] and finally a vasculitic phase [peripheral neuropathy > DAH > GN]. pANCA is only positive in 40% of patients.


Giant Cell Arteritis


  • Most common systemic vasculitis in patients > 60
    • Rare before age 60


  • A granulomatous, large > medium vessel vasculitis with
    • Propensity to for skip lesions –> initial biopsy may be negative
    • Involves the extra-cranial arteries including the temporal artery

Clinical manifestations

There is a classic illness script, but a high # of patients have atypical symptoms

Classic disease

  • Headache – 70%
  • Jaw claudication – 50%
  • Constitutional symptoms – 50%
  • PMR symptoms – 60%

Atypical manifestations – up to 40%

  • Aoritis
    • Arm claudication – subclavian involvement
    • Leg claudication – iliac invovlement
    • Cough – pulmonary A. invovlement
  • Other
    • Mass lesions
    • Fever of unknown origin
    • Seronegative-RA like arthritis


  • ESR – normal in 5%


  • Imaging
    • Ultrasound and MRI – sen 70%, specificity up 100%
      • Skip lesions + halo sign [vessel wall edema] are highly specific


  • Temporal artery biopsy – 90% sensitivity
    • Empiric steroids do not reduce the yield of biopsy for 1-2 weeks
    • False negative biopsies may occur due
      • Skip lesions –> contralateral biopsy
      • Sparring of the temporal artery; tends to occur with aortic involvement
        • –> CTA or MRA


  • Vision complications usually occurs months into the syndrome – opportunity to Rx
  • Blindness develops rapidly after the onset of visual Sx —> prolonged visual symptoms without progression to blindness s makes Dx unlikely.


  • High dose steroids upon suspecting the Dx!
  • Maintenance therapy
    • Prednisone daily OR
    • Methotrexate OR
    • TNF-inhibitors


  • An eosinophilic vasculitic disorder than is predominatly seen in middle age caucasians
Risk factors
  • M=F
  • Background of atopic features for decades
  • 90% of all ANCA vasulitis is seen in Causasians.
Clinical manifestations — Overview
Atopy – 30s
  • Asthma (90% of patients)
  • Allergic rhinitis
  • Nasal polyps 50%
Eosinophilia – usually 40s
  • Symptoms of end-organ complication begin to devlop (GI, Pulm> Card)
Vasculitic phase – 50s
  • Paradoxical improvement in asthma
  • Constitutional symptoms
  • Peripheral neuropathy (70%), DAH (10%), GN (25%)
Clinical  manifestations — details
Eosinophilia complications
  • GI infiltration — most common in the small bowel
  • Lung disease
    • Asthma
    • Fleeting pulmonary infiltrates
    • Upper airways disease – sinus/nasal polyps
  • Cardiac disease (endomyocardial fibrosis) – 45%
*These patients are likely to be ANCA negative and symptoms overlap much more closely with HES (hematolgic causes)
  • Peripheral neuropathy (mononeuritis multiplex) – common
  • Purpura – common
  • GN – 25%
  • DAH – 10%
*ANCA positive more likely.
*Coronary vasculitis also occurs.
*Mesenteric vasculitis (perforation and acalculous CCY)
  • Involves careful exclusion of other causes of eosinophilia
  • Exclusion of hematologic causes is the most challenging (T, B cell lymphoma and HES) particularly in patients with more eosinopilic related manifestations of eGPA [more likely to p-ANCA negative]
  • ANCA – 40% of patient are positive
    • 90% pANCA, 10% ANCA
  • IgE (non-specific elevation)
  • IgG4 (also elevated in disease)
  • Eosinopihilic vascular inflammation
  • eosinophilic extravascular granuloma Granuloma (pathongomnic finding)
*These changes are absent in biopsies from kidney and nerve
  • Prompt response to steroids


VA intern report 4.19 – bronchiectasis, asthma + syndromes and eosinophilia!

Case summary

Thanks to Jake for presenting a fascinating case of a 26M w/ developmental delay and chronic respiratory disease of unclear etiology presents with an exacerbation found to have hypereosinophilia and ultimately diagnosed with ABPA!

Top pearls

  1. There are numerous causes of eosinophilia [see below]. Hypereosinophilia, defined as persistent Eo’s > 5000, has a much more limited DDx = invasive parasitic disease, eGPA and malignancy-related. This degree of eosinophilia requires prompt evaluation for end-organ damage, especially cardiac disease.
  2. Refractory asthma symptoms are often due to inappropriate inhaler technique and/or allergen exposure. In patients with refractory symptoms, consider other causes of wheezing [=wrong Dx, below] or asthma plus syndromes including allergic bronchopulmonary aspergillosis.
  3. ABPA complicates 2% of bronchial asthma and 15% of cystic fibrosis patients. The core features of this diagnosis are hypersensitivity to aspergillus [via skin testing] and significant immunologic reaction [IgE > 500 or 1000]. Central bronchiectasis and fleeting alveolar infiltrates are relatively unique radiographic manifestations of this disease.



Approach to refractory asthma 


Here’s an evernote about ABPA

Here is one approach to bronchiectasis


VA morning report – 4.16 – Brain masses: cancer versus abscess

Case summary

Thanks to Hailyn and Izzy for presenting a fascinating case of a 78M who presented with transient episodes of confusion found to have multiple CNS lesions concerning for cancer > abscess.

Top pearls

  1. Sudden onset of symptoms is often due to obstruction [e.g. ACS] , perforation [e.g., bowel perforation], or electrical disease [e.g, seizure].
  2. There are numerous causes of a brain mass. Malignancy, brain abscess and demyelinating disease are the most important considerations. Radiation necrosis, vascular formations, and contusions are other less common causes.
  3. The majority of patients with metastatic disease to the brain have a readily identifiable primary tumor. In the 10% that don’t, lung cancer, melanoma and colon cancers are the most frequently uncovered tumors.
  4. The majority of patients with a brain abscess are afebrile! Headache and subtle neurologic findings are the most common complaints.

Sudden onset – approach


Brain mass  – approach


Evernote about metastatic disease to the brain:

Brain abscess – approach


VA morning report 4.9 potpourri – heart failure, drug eruptions, neck masses and cervical lymphadenopathy!

Case summary

Thanks to Jake and Hailyn for presenting two fascinating cases this morning.

Jake told us about a 55M w/ remote history of idiopathic cardiomyopathy who developed a morbilliform photodistributed drug eruption possibly from atorvastatin.

Hailyn told us about a case from her recent time in Kenya – a 35M w/ HIV who presented with cervical and supraclavicular LAD due to Tb versus lymphoma.

Top pearls

1. While there is a long list of causes of HFrEF, four causes account for the vast majority – ischemia, valvular disease, hypertension and toxin. Goop reminded us that assigning causality to these entities can be challenging  – does HTN + CHF mean the patient has HTNsive heart disease?

2. Remember that the cornerstone for pharmacologic therapy for HFrEF include – ACE inhibitor, beta-blocker +/- aldosterone receptor blocker. Aspirin and atorvastatin are reserved for ischemic heart disease or are prescribed for a separate condition [e.g., hyperlipidemia].

3.  Does it itch, hurt or bleed? Pruritis [suggesting contact dermatitis, scabies, or atopic reaction], pain [suggesting skin necrosis from SJS/TEN or vasculitis] and bleeding [suggesting a dermal process] are three helpful questions to ask that help filter an otherwise long DDx for a rash.  Assessing for mucosal involvement and looking for exposures [e.g. new soaps, detergents etc] is also important.

More about HFrEF, neck masses and cervical LAD below.

Approach to HFrEF


*Important caveat – all causes of a normal EF can progress to a reduced EF.

Here is one approach to neck masses

The physical exam and imaging [U/S or CT] can really help narrow the DDx.



Here’s one way of breaking down lymphadenopathy



VA morning report 4.2.18 – pancytopenia and AKI!

Case Summary

Thanks so much to Anne Montgomery for presenting a fascinating case of a 74M w/ HIV, and CKD who presented with worsening anemia, thrombocytopenia and AKI on CKD. The work up is still pending, but based on the peripheral smear, there is concern for a primary bone marrow syndrome like MDS.

Top pearls

  1. There are many causes of anemia and thrombocytopenia. As internists, our job is to evaluate for rapidly destructive causes [e.g., DIC, ITP]. If a bone marrow syndrome is more likely, our toolbox is limited to assessing for toxins [e.g., EtOH], meds [e.g., cellcept] and nutritional deficiencies [e.g., B12]. While evaluation for these causes is underway, the peripheral smear can help gauge timing of heme/onc involvement for a bone marrow. Concerning smear -> early heme/onc consult.
  2. The differential for large kidneys on ultrasound includes – HIV associated nephropathy, early diabetic nephropathy, ADPKD, and infiltrate disorders including sarcoidosis
  3. Remember that assessment of intra-renal AKI also includes some serum tests  such as  SPEP/SFLC for myeloma/AL, CK for rhabdo, uric acid for tumor lysis, and the peripheral smear for MAHAs.


Here is one approach



Approach to AKI

Note all the serum tests that may be  needed for intra-renal AKI.