Up in smoke: An unusual case of diffuse alveolar hemorrhage from marijuana

1Introduction

Diffuse alveolar hemorrhage (DAH) is a serious and life threating condition, characterized by the presence of new pulmonary infiltrates, hypoxemia and hemoptysis. It results from bleeding within the lung parenchyma from a variety of pathologies, including autoimmune process, infections, malignancy, cardiovascular disease and illicit drug use [1]. Illicit drug use can cause diverse pulmonary manifestations depending upon the specific substance used, mode of delivery, duration of use, and presence of additives [2]. Marijuana use in US has doubled in the past decade, and there are currently more than 22 million users [3]. DAH has been described as an immediate complication of inhalation drugs, particularly associated with cocaine and synthetic marijuana [4,5]. Here we describe a case of DAH following binge smoking of non-synthetic marijuana.

2Case report

A 21-year-old male was admitted with the acute onset of hemoptysis. The night prior to admission he had smoked several (>5) marijuana joints and subsequently developed blood streaked sputum that became bloodier over time. He presented to ER found to have in no distress but was coughing up blood. Vital signs: Blood pressure 122/84 mmHg, Pulse 92 bpm, respiratory rate 20/ minute, with an oxygen saturation of 98% in ambient air. He was alert and oriented without any evidence of oronasal bleeding. His respiratory exam revealed diffuse rhonchi, remainder of his exam was unremarkable.

Additional history was significant for 2 days of nasal congestion and headaches but no fever, chills, sweats, myalgia, sore throat, skin rashes, or joint pain/ swelling. He reported smoking 2–5 non-synthetic marijuana joints per day (though denied use of any inhalant aid, i.e. bongs), and had no significant occupational exposures or other illicit drug use.

Initial evaluation included a hemoglobin of 16.4 g/dl, leukocytosis of 30.1 k/μL (83% neutrophils, normalized within 24 hours) and normal platelets. Serum chemistries, renal function, liver function, and coagulation studies were all normal. Urinalysis showed 0–2 RBC/ hpf and urine toxicology screen was positive only for tetrahydrocannabinol and negative for cocaine or any other illicit drugs. A Chest x-ray revealed diffuse patchy infiltrates, verified by a Chest CT showing extensive bilateral ground glass infiltrates with upper lobe predominance (Fig. 1) and (Fig. 2).

Fig. 1

CT scan of chest showing bilateral infiltrates.

Fig. 1

Fig. 2

CT scan of chest showing again diffuse infiltrates.

Fig. 2

The patient was started on empiric antibiotics (piperacillin/tazobactum, vancomycin and ciprofloxacin). Infectious work up, including blood and sputum cultures, legionella urinary antigen, quantiferon TB test, and HIV antibodies were all negative. A respiratory viral panel was positive for rhinovirus. Echocardiogram was completely normal. Flexible bronchoscopy was performed and revealed blood-streaked secretions diffusely. Successive bronchoalveolar lavage (BAL) was performed in the right and left upper lobes (RUL, LUL), and both appeared consistent with DAH (Fig. 3, Fig. 4). Cell counts were remarkable for a RBC of 44000 cells/μl with 380 white cells /μl (79% macrophages) from the RUL, and RBC of 37000 cells/μl with 363 white cells (74% macrophages) from the LUL. BAL stains and cultures were all negative, and cytology revealed only erythrophages and hemosiderinophages. An extensive rheumatological serologic evaluation including (ESR, CRP, C-ANCA, P-ANCA, Anti-GBM, rheumatoid factor, complement levels, and ENA panel) were negative. Urine cytology did not show any dysmorphic RBCs.

Fig. 3

Broncho-alveolar lavage of Right upper lobe (RUL) of lung.

Fig. 3

Fig. 4

Broncho-alveolar lavage of left upper lobe (LUL) of lung.

Fig. 4

The patient's condition improved with resolution of the hemoptysis, and he was discharged in stable condition. Outpatient pulmonary function testing was normal and a repeat Chest imaging had normalized. He was counseled to avoid smoking marijuana and remained symptom-free at his follow up visit.

3Discussion

DAH can present as a spectrum of nonspecific symptoms ranging from cough, dyspnea, and hemoptysis to severe hypoxemic respiratory failure requiring mechanical ventilation. Diagnosis is confirmed by bronchoscopy when successive BAL aliquots show progressively hemorrhagic return, and there are iron laden macrophages on cytology [6,7].

Inhalation injury as a cause of DAH has been associated with illicit drug use, especially cocaine, amphetamine and synthetic cannabinoids [8]. Repeated deep inhalation followed by Valsalva maneuver may increase intra alveolar pressure resulting in injury to the alveolar-capillary membrane leading to hemoptysis, pneumothorax, pneumomediastinum and non- cardiogenic pulmonary edema [9,10]. In addition, marijuana inhalation involves a 66% larger volume, 40% deeper inhalation, and 4 times longer breath hold when compared to smoking tobacco [8]. This technique could predispose to inhalation injury.

Only three cases of DAH associated with marijuana use have been described in the literature, two cases after inhalation of synthetic cannabinoid [11,12]. And one case after using a bong made of homemade plastic materials [13]. Our case is unique in that this patient was smoking non-synthetic marijuana and was doing so without the use of any inhalation aids or techniques. It's possible that the rhinovirus URI may have predisposed him to airway inflammation and then the significant marijuana inhalation resulted in inhalational injury. An extensive work-up for other causes of his DAH was unrevealing and his symptoms resolved without treatment. It's worth noting that rhinovirus has not been associated with DAH.

This case highlights a potential new complication from marijuana inhalation that should be considered in the differential diagnosis of patients presenting with DAH. The mechanism by which marijuana might lead to DAH warrants further investigation.