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A Case Cracked

Published on Nov 29, 2015

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PRESENTATION OUTLINE

A Case Cracked

Sumir Shah MSc & Julie Endrizzi MD
Photo by paurian

CC: "Influenza"

  • G.C. is a 45 y.o.male with a PMHx of GSW presenting with chest pain, cough, fevers, and chills that started acutely this morning. Called EMS because was concerned about the flecks of blood in his cough; was given 324 ASA en route.
  • Vitals T35°C BP122/81 P110 RR18 96% on RA

what else do you want to know?

  • Cough with flecks of blood in yellow phlegm x1 day.
  • Fever, chills, diaphoresis x1 day.
  • Mid-sternal, non-radiating, pleuritic chest pain x1 day.
  • Marijuana user. Denies any other illicit drug use.
  • Denies any seizures, LOC, or urinary symptoms
Photo by tom chandler

Physical Exam

  • Gen: AAOx3, uncomfortable HEENT: PERRL, moist mucus membrane CV: RRR s1s2 no murmur, rubs, gallops Pulm: diffuse b/l rales Abd: soft. nontender, nondistended Skin: diaphoretic, no burns

Differentials?

Photo by Stéfan

Untitled Slide

  • Pneumonia
  • URI/Sepsis
  • Barotrauma/Mallory - Weiss
  • Pulmonary Edema
  • Aspiration Pneumonitis
  • ARDS
  • Acute Eosinophilic Pneumonia
  • Malignancy
Photo by zeevveez

Labs

  • Na 140/ K 4.3/ Cl 101/ HCO3 21/ BUN 17/ Cre 1.24/ Glu 119
  • WBC 36.4/ Hg 13.1/ Hct 41/ Plt 277
  • Lactate 2.9
  • ESR 26
  • Utox: + THC, +Cocaine
  • UA: 1+ ketone, 2+ blood, Protein 30, WBC 2, 1+ bacteria, 1+ Squamous Epi

Untitled Slide

New diffuse groundglass opacification of the bilateral lungs, with
tiny centrilobular nodules. Normal cardiac silhouette. The differential diagnosis includes viral
pneumonia, PCP, pulmonary hemorrhage, pulmonary edema, and pulmonary
alveolar proteinosis.

Untitled Slide

1. Diffuse bilateral alveolar groundglass opacities with interlobular
and intralobular thickening, which may represent ARDS, bacterial
pneumonia, or pulmonary alveolar proteinosis (PAP). Recommend
followup when the patient's symptoms have improved to document
resolution.
2. Mediastinal and right hilar lymphadenopathy, which is nonspecific,
but may represent a reactive or infectious etiology.

Untitled Slide

Diffuse Alveolar Hemorrhage

secondary to crack cocaine

The 3 histologic patterns of DAH

  • Pulmonary capillaritis
  • Bland pulmonary hemorrhage
  • Diffuse alveolar damage

Pulmonary Capillaritis

  • Neutrophilic infiltration of the alveolar septa leading to necrosis
  • Behçet's syndrome, Cryoglobulinemia, Wegener's, Henoch-Schönlein, Goodpasture's, RA, SLE, Leptospirosis, UC, endocarditis, Acute Lung Injury, MCTD
  • Drugs: Hydralazine, PTU, Carbimazole

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Vasculitis?

  • Wegner's- upper respiratory tract, lungs, and glomerulonephritis, + C ANCA
  • Churg strauss-chronic rhinosinusitis, asthma, and peripheral blood eosinophilia, + P ANCA
  • Goodpasture's- Anti-GBM, Lungs and glomerulonephritis
  • Henoch-Schönlein- skin, GI, arthritis

Bland Damage

  • Hemorrhage into the alveolar spaces without inflammation or destruction of the alveolar structures
  • Causes include: Anti GBM, SLE, Anticoagulant therapy, Promyelocytic leukemia, Mitral Stenosis/Regurgitation Thrombocytopenias (ITP, TTP, HUS)

Diffuse Damage

  • Edema of the alveolar septa and by formation of hyaline membranes that line the alveolar spaces
  • Causes include: infectious/viral ARDS, polymyositis, SLE, Amiodarone, Amphetamine, Crack cocaine, Cytotoxic drugs, Isocyanates, Nitrofurantoin, Penicillamine PTU, Sirolimus, Trimellitic anhydride

Crack Lung

  • 25 to 60% of crack users present with respiratory symptoms
  • Cocaine blocks the presynaptic reuptake of the neurotransmitters dopamine and NE, leading to severe vasoconstriction.
  • Cocaine also causes direct alveolar cell damage
typically develop in 1-48hr

Most common are edema due to increased capillary permeability and alveolar hemorrhage

also watch for severe barotrauma from valsalva and bronchoconstriction in preexisting asthma patients

cocaine users unable to kill bacteria with macrophages and nitric oxide, increasing risk of pulmonary infection
Photo by Marco Gomes

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Endothelin (ET-1) also increased and possibly a measure of alveolar damage

Toxins/Adulterants

  • Butyrfentanyl
  • Levamisole, an anti-helminthic, can cause an +ANCA vasculitis
  • Other common adulterants (talc, mannitol, tetracaine, lidocaine, procaine) are not associated with DAH
Photo by Marco Gomes

Clinical Presentation

  • Cough, hemoptysis, fever, & dyspnea
  • CXR is nonspecific patchy/diffuse opacities, abnormal R heart border in Mitral stenosis. Less likely to exhibit Kerley B lines, pleural effusions, and peri-bronchial cuffing as in edema
  • CT findings are ground glass opacities that are diffuse and b/l
  • Labs are often nonspecific
hemoptysis absent in 33%
Photo by Heo2035

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DAH

New diffuse groundglass opacification of the bilateral lungs, with
tiny centrilobular nodules. Normal cardiac silhouette. The differential diagnosis includes viral
pneumonia, PCP, pulmonary hemorrhage, pulmonary edema, and pulmonary
alveolar proteinosis.

Diagnosis

  • DLCO >100% is a sensitive finding if patient can tolerate PFTs. Due to increased hemoglobin in the alveolar space, which removes CO from the exhaled air
  • Bronchoalveolar lavage is gold standard
  • Antibodies if suspicious of vasculitis
  • Biopsy
diagnosis is primarily clinically based on HPI
Photo by jetheriot

Treatment

  • Cessation of implicated drugs and exposures, treatment of infection, and reversal of excess anticoagulation are key
  • O2, methylprednisone (500-2000mg x 5 days IV followed by prednisone 1mg/kg PO), and cyclophosphamide are mainstays
For drug-induced DAH, in addition to cessation of the culprit drug, we suggest systemic glucocorticoid therapy due to the severity of the disease and the histopathologic observation of inflammation in some patients (Grade 2C).

weak, observational recomm
Photo by Caza_No_7

Disposition

-Patient was transferred to highland then d/c on corticosteroids
Photo by minnepixel