INHALANT ABUSE AND RESPIRATORY FAILURE. Chalita Waenlor, MD

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1 INHALANT ABUSE AND RESPIRATORY FAILURE Chalita Waenlor, MD

2 Inhalants Substances with significant acute and chronic toxicity. Wide variety of chemical structures with the majority being hydrocarbons (aliphatic, aromatic, or halogenated), nitrites, or nitrous oxide. Inhalants are similar in that they are all volatile substances, highly lipid soluble, and readily absorbed across the pulmonary bed

3 Inhalant abuse is a common problem in adolescents due to several factors: Inhalants are readily accessible: An average home has between 30 and 50 products with abuse potential. They are inexpensive and legal to buy and possess. The perceived risk of use is low

4 Technique Sniffing : sniffed directly from a container or sprayed directly Huffing : inhaled from a saturated cloth that is held under the nose or near the mouth Bagging : inhaled from a bag that is placed over the mouth, nose, or head

5 Toxicity Respiratory Cardiovascular Central nervous system Peripheral nervous system Gastrointestinal Hepatic Renal Hematologic Immunologic Dermatologic

7 Mechanism of pulmonary injury Not fully understood. Physiologic abnormalities in lung mechanics (decreased compliance and total lung capacity) Pathologic changes such as interstitial inflammation, polymorphonuclear exudates, intraalveolar edema and hemorrhage, hyperemia, bronchial and bronchiolar necrosis, and vascular thrombosis. Reflect both direct toxicity to pulmonary tissue and disruption of the lipid surfactant layer

8 Pulmonary toxicity Asphyxia : may result from suffocation (bagging) as well as displacement of oxygen in the alveoli Bronchospasm Necrotizing chemical pneumonitis Lipoid pneumonia hemorrhagic pulmonary edema Pneumothorax Subcutaneous emphysema of the chest wall Pleural effusion Empyema Secondary bacterial or viral infection

9 Pulmonary toxicity Pulmonary manifestations occur within 30 minutes after aspirate but may be delayed for 12 to 24 hours. Immediate signs of aspiration include coughing, choking, gagging, and vomiting.

10 Physical examination Vary with the degree of pulmonary injury and may include : Tachypnea Dyspnea Cyanosis Wheezing Diminished resonance on percussion Tubular breath sounds Rales

11 Diagnosis Hypoxia : present on pulse oximetry and electrocardiograms may reveal arrhythmias. CXR : reveal evidence of aspiration, infiltration or pneumothorax

12 Initial: Patchy densities appear in basilar areas of both lung fields with increased interstitial markings and peribronchial thickening.

13 Day 2: More extensive diffuse alveolar infiltrates are apparent.

14 Day 6: Dense consolidation and atelectasis are evident in the right lower lobe.

15 Treatment Supportive and includes oxygen and close monitoring of respiratory status. Bronchospasm should be treated with selective beta-2 agonists. Endotracheal intubation and conventional mechanical ventilation are indicated in patients with respiratory failure. Consider ICD insertion if pneumothorax.

16 Treatment Corticosteroids have shown no beneficial effect on the course of hydrocarbon aspiration in observational studies and may be harmful. Clinical findings often worsen over the first several days but typically resolve within a week.

17 Treatment Pneumonitis caused by hydrocarbon aspiration should not be treated routinely with antibiotics unless signs of secondary infection, including the following, are present: Recurrence of fever after the first 48 hours Increasing infiltrate in chest radiograph Leukocytosis after the first 48 hours Sputum or tracheal aspirate positive for bacteria

18 CASE REPORT

19 TOLUENE INDUCING ACUTE RESPIRATORY FAILURE IN A SPRAY PAINT SNIFFER Am J Case Rep, 2012; 13: 92-95

20 Background Toluene is an aromatic hydrocarbon. Acute and chronic exposure affect the central nervous, cardiovascular, renal, and gastrointestinal system. Also produces severe acid-base and electrolyte disturbances.

21 Background Report a rare case of a chronic toluene abuser presenting with generalized muscle weakness and developed acute respiratory failure

22 Case report A 27 yr male presenting with an acute episode of severe generalized weakness, 3 episodes of vomiting. There was not reported use of any drug or medication. He admitted having a similar, but less severe episode few weeks before which resolved with no intervention.

23 Physical examination V/S : HR 101 bpm, RR 22 bpm, BT 98.4 F, BP130/74 mm Hg, and O2 sat 96% on 2 LPM. Alert and oriented with mild distress due to weakness. Neurological examination : flaccid extremities with profound motor weakness 1/5 and hyporeflexia.

24 Initial laboratory data K 1.5 mmol/l, CO2 14, Ca 9.2 mg/dl, Mg 3.0 mg/dl ALP 297 IU/L, ALT 70 IU/L, AST 51 IU/L BUN 5 mg/dl, Cr 1.0 mg/dl, CPK 615 IU/L Urine ph 5.5 EKG : sinus tachycardia with intra-ventricular conduction delayed, QTc prolongation of 702 ms, and Q waves in inferior leads

25 Admission EKG

26 Initial treatment Potassium chloride iv Lactated Ringers Admitted ICU for close monitoring

27 Treatment ( cont. ) 6 hrs later, he developed severe respiratory distress and hypoxia. He was intubated and placed on ventilatory support. ABG on FiO2 100% : ph 7.026, pco mmhg, po mmhg, and HCO mmol/l. Serum K still 1.5 mmol/l, PO4 1.2 mg/dl, CO2 15 mmol/l and Cl 119 mmol/l. Tx : Aggressive replacement of K, PO4 and NaHCO3 iv drip

28 Additional workup results

29 Problem list Hypokalemic muscular paralysis. Acute respiratory failure. Elevation of transaminases Hypophosphatemia Hyperchloremic non-anion gap metabolic acidosis. Acute renal failure.

30 At ICU After 16 hrs of intubation, he started recovering his strength. He was able to move all extremities and also remove his ET-tube by himself. Fortunately, no sign of respiratory distress, and respiratory and hemodinamically stable.

31 More history taking He confessed being a spray paint sniffer for the last 15 yrs at least 3-4 times/wk. A spray paint : one component was toluene. Hippuric acid level in urine ( confirm toluene toxicity ) : 8.0 g/l (normal <5.0 g/l).

32 He admitted for 5 days on continuous electrolyte replacement and periodic monitoring. His clinical condition improved rapidly as well as all abnormalities found in the initial workup and electrocardiogram.

33 Discharge EKG

34 Discharge and follow-up Discharged with advice to avoid paint spray sniffing and close follow-up with the outpatient clinic. Unfortunately, he never had any follow-up, but he had an ER visit 6 mo afterwards for an episode of foot cellulitis. During this visit blood work still showed low K 2.8 mmol/l.

35 Discussion Toluene : aromatic hydrocarbon. Main compounds of glue, gasoline, acrylic paints, varnishes, lacquer, paint thinners, adhesives, and so forth. Widespread cause of intoxication is sniffing. Incidence of solvent abuse is rising and has reached epidemic proportion in some countries. Increased prevalence among children and adolescents.

36 Discussion Toluene accumulates in adipose tissues when absorbed by skin or ingested due to its hydrophilic properties. It is rapidly cleared via the lungs when inhaled.

37 Discussion Toluene uses the cytochrome P-450 system in hepatocytes for its metabolism. It is then metabolized to benzyl alcohol that is more water soluble. An oxygen atom is inserted to it by alcohol dehydrogenase to form benzoic acid. Benzoic acid is conjugated to hippuric acid by adding a glycine group in the hepatocyte mitocondria. Hippuric acid is the byproduct of toluene that may be used as an indirect measure of toluene level.

38 Discussion Multiple effects depend on the concentration and length of exposure. Although CNS appears to be the most sensitive to its effects, the rest of systems might be also affected. There are several reports describing cardiovascular, renal, and gastrointestinal effects as well as acid-base and electrolyte disturbances which have been so severe to produce death.

39 Discussion Chronic toluene sniffer presenting with severe generalized weakness acute respiratory failure elevation of transaminases non-anion gap metabolic acidosis acute renal injury

40 Discussion He was treated with Aggressive K and PO4 replacement for hypokalemia and hypophosphatemia Ventilatory support for respiratory failure Bicarbonate infusion for severe acidosis and urine alkalinization Fluid supplementation for AKI.

41 Discussion The effects of toluene toxicity in this patient are clear. He developed many of them such as nonanion gap metabolic acidosis which is the result of overproduction of hippuric acid. This is an indirect way of sodium bicarbonate loss in the urine due to the binding of the conjugate base of hippuric acid and sodium or potassium.

42 Discussion Another toluene effect seen is distal tubular acidosis (RTA) type 1 potassium wasting in the urine severe hypokalemia, hypophosphatemia urine ph greater than 5.5 and positive urine anion gap due to low excretion of NH4+. potassium wasting might be explained by the same mechanism of potassium binding to bicarbonate and then excrete in the urine.

43 Discussion In this case, hypokalemia may due to chronic low K intake or extra renal losses. The measurement of K was done in a spot urine sample. The best way to quantify it is with 24-hour urine collection which would show the real amount of K wasted. His urine anion gap was negative which also goes against RTA

44 Conclusions There are multiple systemic effects of chronic toluene exposure. Acute respiratory failure is a rare complication that may be lethal. Patient who presents with unexplained hypokalemic muscular paralysis along with renal tubular acidosis with or without respiratory failure should be questioned about the possibility of toluene abuse.

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