![]() A dab of BHO on the end of the metal wire would then be touched against the nail causing an instant vaporization. The nail would be heated with the propane blow torch until it became bright red in color temperatures ranging from 900 to 1075☏. Our patient described her process of inhaling BHO with the use of a “Maverick” glass water pipe, 4-5-inch-long titanium cylindrical piece known as a “nail”, a propane blow torch and a small metal wire to hold the dab. When sold legally at a dispensary in a state where cannabis is legalized, such as Oregon, the guidelines state the level of butane must be less than 5000 ppm. Individuals using an unregulated street product can be inhaling up to 75% THC, compared to 5–20% THC in traditional smoked cannabis, and an unknown level of pure butane and terpene ranging from 0.1 to 34%. When made illegally there are no guidelines that dictate an acceptable level of butane remaining in the product. The bowl is then placed on a hot surface to allow for the partial evaporation of the butane leaving behind a sticky brown substance, similar in texture to wax, which is then known as BHO. ![]() This allows the liquid remnants of THC, one of the psycho-active ingredients in cannabis, and butane to pass into a bowl. A filter is used at one end of the glass tube which entraps the large pieces of cannabis. It begins with “blasting” or spraying liquid butane through a glass tube containing dry cannabis. Our patient described the meticulous and very dangerous process of producing BHO. A bronchoalveolar lavage (BAL) was not part of the workup, however if the patient showed signs of lipoid pneumonia (subacute onset with hemoptysis, chest pain, and fever or with markedly dense nodules on CT) a BAL would be useful to exclude this diagnosis, characterized by lipid-laden macrophages.ĭab, or dabbing, is the colloquial street term used by individuals that inhale butane hash oil, named in part to the small amount of BHO used each time. Ongoing severe hypoxia prompted further work up of allergic bronchopulmonary aspergillosis (ABPA), alpha-1 antitrypsin deficiency, HIV and influenza however, all tests were negative. Arterial blood gases showed a pH of 7.43, pCO2 of 29.1 mmHg, pO2 of 73 mmHg and an HCO3 - of 19.3 mMol/L. Sputum gram stain and culture were negative. Initial labs revealed leukocytosis with a WBC count of 23.8 thou/mcL with a neutrophil predominance of 18.7 thou/mcL and eosinophilia of 1.6 thou/mcL. Due to the severity of her respiratory distress a CT angiogram with PE protocol was completed no evidence of a PE was found, however the scan demonstrated bilateral patchy infiltrates (see Figs. 1) indicating mild hyperinflation without any acute pathologic process. Work up included a PA chest x-ray (see Fig. She was treated with breathing treatments, antibiotics, IV steroids and Tamiflu although influenza titers were negative. She was admitted to a different hospital one month prior for similar symptoms. She has a 1-pack year smoking history and stated she had smoked marijuana infrequently in the past. Respiratory auscultation demonstrated decreased air entry with diffuse expiratory wheezing, bilateral rhonchi and a prolonged expiratory phase with obvious use of accessory respiratory muscles. On physical exam she was noted to be tachycardic and tachypneic. She further complained of a productive cough, nausea and headache. She was initially given three breathing treatments, IV steroids and oxygen with an FiO2 of 36% via nasal cannula, however, remained hypoxic saturating at 90%. She was found to have acute hypoxic respiratory failure with oxygen saturations of 89% at rest and 79% during ambulation, while on room air. A previously healthy 18-year-old female presented to the Emergency Department with complaints of shortness of breath for 3–4 days.
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