The Danger of Diagnostic Momentum…

Author: The Infamous Peter Gruber, MD
(Cases initially presented by Carlo Lutz, MD)

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3 cases leading you down the garden path…

Case 1:

42 y/o M p/w black stools and, blurred vision; taking NSAIDs and ASA. Rectal exam with melena. BP: 163/95, HR: 79, RR: 18, Temp: 98.5F. There was a momentum for GI bleed due to patient taking NSAIDs and ASA.

HOWEVER- blurred vision, elevated Cr of 1.9; Hb of 10.7; Platelets of 13 and an elevated LDH of 1833.

• Platelets of 13 indicates this is not a simple NSAID induced GI bleed

• Patient was transfused platelets and has increasing elevation of LDH and develops rash

• Blood smear shows schistocytes and diagnosis of TTP is confirmed by lack of ADAM13 (which leads to excessive aggregation of platelets)

• Initial HIV test was negative but a subsequent HIV test was positive

• There is a rare HIV associated TTP, which tends to occur with CD4<200
  • This has a 90% mortality if untreated but is highly responsive to plasma exchange

• This patient gets HAART and plasma exchange and does well

Gruber’s Musings:

• Missing the diagnosis: you can easily be led down the garden path of thinking a GI bleed 2/2 NSAIDs. However, HOW do you explain the very low platelets and elevated creatinine?
  • This is not explained by use of NSAIDs

• What are causes of thrombocytopenia? 
  • Peripheral blood smear will distinguish between true thrombocytopenia and artefactual (ex: platelet clumping):
    • Presence of schistocytes indicates TTP, HUS or DIC
    • Presence of lymphocytosis, atypical lymphs or toxic granulation indicates infection
    • Presence of blasts indicates a primary bone marrow problem
    • Presence of none of these goes along with isolated thrombocytopenia (ie ITP or drug induced problem ie heparin induced thrombocytopenia(HIT))

• Wrong treatment: second opportunity to blow this case is by seeing low platelets with GI bleed and giving platelets
  • Before giving platelets, one should ask how can giving platelets in thrombocytopenia make a patient worse?
    • Answer: TTP and heparin induced thrombocytopenia(HIT)

• Cognitive Forcing Strategy is an algorithm to force you to avoid missing important diagnosis or making critical mistake in treatment
  • In a case of low platelets where you are considering giving platelets, ask yourself: Could this be TTP or HIT?

• With regards to transfusion of platelets to bleeding patients, recent literature has shown that giving platelets to patient with a GI bleed or head bleed because a patient is on aspirin increases mortality

• TTP has schistocytes on smear and very elevated LDH ie >500
  • If no schistocytes or no significantly elevated LDH, not TTP

• FAT RN mnemonic for TTP maybe should be FLAT RNS:
  • where “L” is for very elevated LDH,
  • where “S” is for Schistocytes and
  • FAT RN for Fever, Anemia, Thrombocytopenia, Renal failure, Neurologic complaint/findings
  • TTP may only have thrombocytopenia and anemia and not fever, renal failure or neuro findings
  • Neuro findings may only be transient so you may need to ask specifically about history of this 

• Why was the initial HIV test neg?
  • It may be that the patient was in the window period before test became positive:

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Case 2:

59 y/o M with diagnosis of asthma in the last 2 weeks presents with increasing dyspnea on exertion. Wheezing on exam. Momentum for asthma exacerbation- ordered for nebulizer treatments and CXR.

HOWEVER- POCUS with b/l B lines; CXR with CHF; pro-BNP of 1802; and eventual inpatient echo shows an atrial myxoma.

Gruber’s Musings:

• Be suspicious of a patient who develops asthma at age 59- likely patient has another dx
• All that wheezes is not asthma

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Case 3:

40 y/o F PMHx large fibroids p/w syncope. Menstruating for 4 days with 4-5 pads a day. She notes walking into house feeling lightheaded and then was found on the floor by family. BP: 111/63, HR: 102, RR: 16, Temp: Afebrile, Saturation: 100% on RA. Physical exam with large midline mass (fibroid) and scant blood on pelvic exam. Momentum for syncope 2/2 heavy menstruation.

HOWEVER- H&H of 9/29, Platelets of 180 and normal conjunctivae

• Not particularly low especially for the Bronx in terms of being responsible for syncope and current tachycardia
• Could be a thought that maybe next CBC will show a much lower H&H but the patient has been having bleeding for 2 weeks so H&H likely equilibrated and significant drop in next H&H unlikely

In the meantime, patient had an EKG:

What else are you thinking? Any other tests you want?

• Since scant blood on pelvic and a mild anemia didn’t explain syncope or tachycardia, a D-dimer was ordered and later comes back very elevated with a level of 16 so patient underwent a V/Q study

Gruber’s Musings:

• TWI in anterior or inferior leads are more common with pulmonary embolism than they are with ischemia (especially in a young person)
  • Marriott and Mattu found TWI in inferior and right sided precordial leads specific for PE

• After seeing this EKG, this patient should go straight to CTA, V/Q or Echo rather than getting d-dimer as she is at high risk for pulmonary embolism.  Pt probably should get heparin before going to CTA due to high risk
  • This patient ended up getting Lovenox and is admitted
  • Patient gets TTE while waiting for a bed which shows RV strain and patent foramen ovale (PFO) with a thrombus located through the PFO
  • Patient gets atrial thrombectomy and bilateral surgical pulmonary embolectomy and PFO closure

• This case is similar to a case I had in the past where a woman in her 30s came in with syncope and heavy menstrual bleeding and was tachycardic- seemed like she syncopized 2/2 vag bleeding but her Hb was 11 so that really didn’t explain her passing out or tachycardia. As it turned out, she also had a PE.
• Another case I had was a woman who was brought in unresponsive with vag bleeding with BP 75/40 and a high glucose on FS. Once again, initial momentum was toward exsanguination being her problem but her BP of 75 didn’t explain her unresponsiveness. It turned out she was in diabetic coma with very elevated blood sugar and severe metabolic acidosis so think hard before latching onto diagnosis where there is information that doesn’t support it

• Patients with a pulmonary embolism and PFO are at risk of a paradoxical embolism- an embolism going from the venous to arterial side and travelling to the brain
  • Although the prevalence of PFO is about 25 percent in the general population, this increases to about 40 to 50 percent in patients who have stroke of unknown cause, referred to as cryptogenic stroke.
    • This is especially true in patients who have had a stroke before age 55.
    • In some cases, the PFO combines with another condition, such as atrial fibrillation, to increase the risk of stroke.
  • Increased right heart pressure (i.e. pulmonary embolism) can create an intra-atrial pressure gradient opening the foramen ovale and allowing migration of thrombus through the PFO
• Consider PFO in a patient who reports SOB with Valsalva maneuvers (ex: defecation and urination) as it may transiently create pressures that open the PFO

• Whereas hypoxemia in patients with pulmonary embolism is usually responsive to oxygenation, refractory hypoxemia should raise the suspicion of PFO
  • Positive pressure respiratory support may worsen this hypoxemia as the increase of the intrathoracic pressure can cause opening of the foramen ovale, particularly when high levels of ΡΕΕΡ are applied 
  • Think of PFO in refractory hypoxemia that is unexplained by other causes(ASD), particularly where there is an increase in pressure in the right heart chambers (PE, mechanical ventilation) causing right-to-left shunting.
  • Transcranial doppler may be the the diagnostic procedure for PFO, as it is cheaper, faster to perform and comparable with TEE in terms of sensitivity and specificity

• Patients with pulmonary embolism die of circulatory failure and not ventilatory failure
  • Intubating PE pt will not fix problem and may aggravate it
  • If PE patient is hypoxic or has labored breathing, try high flow nasal cannula
  • If you need to intubate, initiate or escalate pressors beforehand to establish a hemodynamic margin of safety prior to intubation

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