All posts by vmcimchiefs

Lung Cancer

We discussed a case of an elderly woman with extensive smoking history, who presented with chronic dry cough, chronic left upper arm pain, a remote episode of hemoptysis, and subacute dyspnea on exertion, which were all not improved despite a course of antibiotics, found to have a large R pulmonary mass due to Small Cell Lung Cancer.

TYPES OF LUNG CANCER

  • Non-small cell lung cancer (80-90%)
    • Adenocarcinoma
    • Squamous cell carcinoma
    • Large cell carcinoma
    • Staging based on TNM cancer staging
  • Small cell lung cancer (10-20%)
    • One traditional way to stage is based on limited disease vs extensive disease.
      • Limited disease: tumor confined to the ipsilateral hemithorax and regional nodes, able to be confined to a single XRT port
      • Extensive disease: tumor beyond the boundaries of limited disease, including distant metastasis, malignant pleural or pericardial effusion, and contralateral lymphadenopathy

Check out the latest 2021 USPSTF guidelines regarding lung cancer screening:

Immune thrombocytopenia (ITP)

We discussed a case of an elderly man with hypothyroidism and HTN, who presented with acute bleeding from gums, petechiae / bruising, found to have severe thrombocytopenia due to ITP.

FRAMEWORK FOR THROMBOCYTOPENIA

THROMBOCYTOPENIA

  • Mild: 100-150k
  • Moderate: 50-90k
  • Severe: < 50k

ITP

  • Epidemiology
    • 20-30 years (female predominance)
    • > 60 years (more cases in this group)
ITP2

For more information, check out:

Anticholinergic overdose

We discussed a case of a patient with no significant past medical history, who presented with acute seizure-like activity and acute encephalopathy, found to have tachycardia, mydriasis, sluggish pupillary accommodation to light, and urinary retention, due to Anticholinergic overdose. It was discovered that they took > 100 tablets of Benadryl.

Initial evaluation of various toxidromes should be based on clinical findings (vital signs, eyes, skin/secretions, mental status)

Anticholinergic toxicity affects can affect peripherally, centrally, or both.

Treatment

  • Ensure ABCs are intact
  • Cardiotoxicity: sodium bicarb can be used if widened QRS (>100 ms)
  • Decontamination: activated charcoal can be used if the patient presents within the first 2 hrs
  • Seizures / agitation: treat with ativan
  • Physostigmine: may be used if there is both peripheral and moderate central anticholinergic toxicity, but should NOT be given if the QRS is > 100ms or in TCA overdose

Acute eosinophilic pneumonia

We discussed a case about a middle-aged woman with HTN, uncontrolled T2DM, hx of MRSA otitis externa, who presented with subacute myalgias and bilateral leg pain with fevers and chills, found to have MRSA bacteremia and multiple MRSA SSTI / abscesses. Her hospital course was complicated by a drug reaction (rash) to Vancomycin, so she was treated with Daptomycin. Later on, she developed acute hypoxic respiratory failure, peripheral eosinophilia, and found to have acute eosinophilic pneumonia due to Daptomycin.

Eosinophilia
Eosinophils can infiltrate into any organ and cause damage

  • Peripheral absolute eosinophilia > 500
    • Mild: 500-1500
    • Moderate: 1500-5000
    • Severe: >5000

Eosinophilia Differential

Reference: Clinical Problem Solvers

ACUTE Eosinophilic pneumonia

  • Febrile illness
  • < 7 days of nonproductive cough, dyspnea, and diffuse pulmonary opacities
  • Can lead to respiratory failure in hours to short days
  • Diagnosed by
    • Clinical presentation / symptoms
    • Chest imaging
    • BAL with ≥ 25% eosinophils
    • Note: you may not see peripheral eosinophilia during the early stages of disease

CAUSES OF PULMONARY EOSINOPHILIA

  • Toxins (inhalation)
    • Cigarette smoking, dust
    • Cocaine, meth, marijuana, heroin
  • Medications
    • NSAIDs
    • Antibiotics (e.g. daptomycin, sulfonamides)
    • Anticonvulsants (e.g. phenytoin)
  • Infections
    • Parasite (e.g. strongyloides)
    • Fungi (e.g. aspergillus, coccidiodomycosis, cryptococcus)
  • Vasculitis (e.g. EGPA)
  • Neoplasms (e.g. lung cancers, metastasis)
  • Interstitial Lung Disease

MANAGEMENT

  • Treat the underlying cause
  • Glucocorticoids

REFERENCES

Pulmonary eosinophilia

Severe mitral stenosis

We discussed a case about an elderly woman with history of HTN, HLD, CVA, and rheumatic heart disease, who presented with palpitations and dyspnea on exertion, found to have severe mitral stenosis and atrial fibrillation. Unfortunately her hospital course was complicated by bilateral lower extremity arterial thromboemboli.

Rheumatic heart disease is the leading cause of mitral stenosis that affects females more than males (4:1).

Clinical manifestations
Patients can be asymptomatic for years until they develop severe stenosis.

  • Dyspnea (due to pulmonary congestion)
  • Fatigue (due to low cardiac output)
  • LE edema (due to right heart failure)
  • Orthopnea
  • Pulmonary hypertension
  • Systemic embolization

MS and atrial fibrillation
About 50% of patients with MS will have afib.
Without anticoagulation, these patients have a risk of thromboembolism of 20-25%.

Valvular afib = afib in the setting of…

  • Moderate to severe MS OR
  • Presence of a mechanical heart valve

Severity grading

  • A: at risk of MS
  • B: progressive MS
  • C: asymptomatic severe MS
  • D: symptomatic severe MS

Severe MS measurements:

  • Mitral valve area ≤1.5 cm2
  • Mean mitral valve gradient > 10 mm Hg
  • Pulmonary artery systolic pressure > 30 mm Hg

Treatment
If the patient is a candidate, percutaneous mitral balloon valvuloplasty (PMBV) is the treatment of choice.

References

2020 ACC/AHA Guideline for the Management of Patients With Valvular Heart Disease

Eosinophilic Esophagitis

We discussed a case of a young man with history of severe persistent asthma who presents with difficulty swallowing – specifically a sensation of food stuck mid-chest. He has difficulty with solids>liquids. Patient had an EGD showing a “feline” esophagus or ring-like appearance of the esopahgus.

Diagnostic criteria for EOE

  1. Symptoms of EOE
  2. >15 eosinophils on HPF
  3. Exclusion of other causes of EOE including GERD (GERD is thought to increase eosinophils, we often treat GERD and re-test for presence of eosinophils and symptoms before diagnosing EOE however more recently, research shows that EOE and GERD are not mutually exclusive)

Treatment for EOE

  1. Dietary elimination of allergens
  2. PPI
  3. TOPICAL steroids (swallow Fluticasone)
  4. Dilation for symptomatic relief
  5. Recent biologic agents

Patient progressed to have peripheral eosinophilia and worsening persistent asthma. Most patients with EOE have peripheral eosinophilia and high IgE. Due to patient’s persistent asthma, he was placed on a biologic which improved his asthma exacerbations.

Post Infectious GN

We present a middle aged female iwth chronic TPN use via central line after roun-en-y procedure complicated by necrosis and short gut syndrome who presents with subacute malaise. She is found to have Enterococcus faecium and coagulase negative staph bacteremia. She develops an AKI with UA showing hematuria and proteinuria. Urine sediment shows dysmorphic RBC and muddy brown cast. We reviewed the ddx for glomerulonephritis. Due to elevated ANA and normal ANCA, and low compliment levels, patient was diagnosed with post-infectious GN. She had ASO+ titers.

Post infectious GN is uncommon in >40yo. It is usually due to group A strep however can happen with non-strep bacteria, viruses, parasites, fungi and bacterial endocarditis or VP shunt infection. The source of E. Faecium was thought to be due to a line infection and perhaps endocarditis (although TEE was too high risk to confirm diagnosis). Patient received diuresis and had strong recovery.

Angioedema due to Ace-I

An elderly male with alcoholic cirrhosis and metabolic syndrome with long term ace-inhibitor use and recent initiation of alogliptin presenting with acute onset tongue swelling. He did not have any identifiable triggers prior to this including new foods/allergens/insect bites. He was admitted to ICU for airway monitoring. It is important to remember the type of angioedema as the treatment/management will differ. Symptoms that indicate a histamine mediated angioedema include urticaria, flushing, pruritis and bronchospasms. Symptoms that indicate a bradykinin mediated angioedema presents with lack of urticaria or skin rash. You should also ask for family history of episodic swelling or recurrent abdominal pain (angioedema can present in abdominal wall).

Differential diagnosis for bradykinin mediated angioedema includes:

  1. Hereditary angioedema
  2. Acquired angioedema
  3. Ace-I induced angioedema

Treatment for bradykinin mediated angioedema

  1. C1 esterase inhibitor replacement (plasma derived or recombinant types)
  2. Plasma kallirein inhibitor
  3. Bradykini-2 receptor antagonist
  4. FFP

Cardiac Syndrome X

We describe an elderly female who is previously healthy besides an abnormal stress EKG few months ago. She presents with severe chest pain while holding her grand son and improvement in pain with SL Nitro. She had normal EKG and normal troponins. She underwent angiography showing slow flow in all coronary vessels, particularly LAD but no obstruction. She was diagnosed with microvascular angina, sometimes referred to as Cardiac Syndrome X.

Microvascular angina describes coronary microcirculation that are sensitive to vasoconstrictor stimuli and lack capacity to vasodilate appropriately without frank CAD (<50% stenosis). Diagnosis should be suspected in anyone who has episodic chest pain. Patients can have normal EKG between episodes. Some may have mild CAD (<30% stenosis). If they have 30-50%, you will do further testing to measure resistance to blood flow in microcirculation.
Treatment includes risk factor modification for CAD, ASA, Statin, SL nitro PRN and if refractory, BB>CCB.

Euglycemic DKA

We describe a case of a middle aged female with history of DM 2 (treated with Metformin and Jardiance) presenting with abdominal pain, nausea, vomiting. She was found to have colitis on CT scan.

She was also found to have metabolic acidosis with ketosis WITHOUT hyperglycemia. Differential for AGMA included

  • Glycols
  • Oxoproline (acetaminophen metabolite)
  • Lactate
  • D-lactate
  • Methanol
  • ASA
  • REnal failure
  • Ketoacidosis

Patient was diagnosed with Eugylcemic DKA due to SGLT-2 inhibitor, Jardiance or empagliflozin. SGLT-2 work at the proximal convoluted tubule to inhibit reabsorption of glucose and facilitates excretion of glucose into urine. Advantages of SGLT-2 inhibitors include weight loss, reduced blood pressure, reduced CV mortality and improved renal outcomes in those w/ nephropathy. Disadvantages include risk for UTI and GU fungal infections, increased urine output (hypotension/dehydration) and a questionable increased risk for amputation.

Below is a summary for other Anti-glycemic agents that can be used.