• Understand the central nervous system effects common to all hydrocarbons.
• Understand the individual toxicity of the toxic alcohols and how their metabolism affects this.
• Understand the general management of patients poisoned by hydrocarbons.
• Detail specific management required for individual hydrocarbons.

A 34-year-old male is brought to the Emergency Department by ambulance. The available history is that he ingested between 300 and 700 mls of antifreeze 1 hr 50 min ago and co-ingested with 3 glasses of wine. This was an impulsive act after an argument with his partner.

His only medications are carbamazepine 200 mg tds for post-traumatic epilepsy.

In transit he was initially awake and alert, with a pulse rate of 125/min and a blood pressure of 90/60. He had a brief grand mal seizure en route. On arrival in the ED he had a second tonic clonic seizure, following which he was noted to be disorientated to time. His pulse rate was now 125/min and BP 125/48. Arterial blood gases were as follows:

• pH 7.30
• pO2 296
• pCO2 37
• Bic 19
• BE ‑7

Biochemistry testing revealed:

• Na 144, K 3.5
• Urea 5.8
• BSL 5.3
• Ethanol 36.3 (0.17 gm%)
• Osmol 375

1. What is the osmolar gap?
2. What further investigations are required?
3. What chemical could be involved here?
4. Can you calculate a possible blood concentration? Does this explain the patient’s condition?
5. What decontamination is indicated?
6. What treatment is required?
7. Is there an effective antidote? How is it administered?
8. Are the any effective mechanisms for enhancing clearance? If so, what additional measures must be undertaken?
   The following day these results were obtained:
   Na 143, K 3.8, Urea 3.0, BSL 5, Ethanol 35.7 (0.16 gm%), Osmol 335.
9. What are the end points for the different treatments employed here?

A 39-year-old male Russian sailer is brought to the Emergency Department. He has been drinking heavily in his fishing boat and is grossly intoxicated and unable to walk.

On arrival in ED he is agitated, sweaty and complaining of abdominal pain. His pulse is 120/min, respiratory rate 30, BP 150/100 and Sat PO2 99% on room air. He has mottled skin.

Thirty minutes after presentation he fits, becomes bradycardic with a pulse of 39, and hypotensive 90/. He is intubated and ventilated.

ABG performed at that time reveal:

• pH 6.7
• CO2: 12
• O2: 150
• HCO3: 3
• Base Excess –34

Biochemistry is: lactate 11, Na 146, K 4.2, Urea 5.9, Cl 109, Glucose 5, Anion Gap 36, Osmolality 361

1. What is the osmolar gap?
2. How would you characterised or describe the acidosis?
3. What possible toxicological and non-toxicological causes should be considered?
4. Is decontamination indicated?
5. What management is required?
6. What investigations, including the results, are required prior to the institution of the definitive treatment?
7. What is the definitive treatment?
   The container he has been drinking from is brought in from the boat. The label is in Indonesian; ‘ALKOHOL’ is the only recognisable word
8. What is the most likely chemical involved here?

A 16-year-old female is brought to hospital by ambulance. The history given is that she was at a party and drank a bottle of vodka in approximately 30 minutes. Over the following hour she became progressively drowsy. She did not vomit.

Currently she withdraws to pain, does not open her eyes and is not vocalising. She has been incontinent of urine. Her pulse is 120/min and blood pressure 90/40. Her respiratory rate is 10/min and shallow. Oxygen saturation is 94% on room air.

1. What immediate management is required?
2. Is decontamination indicated? If so, how?
3. What investigations are indicated?
4. What are the possible reasons for her reduced level of consciousness?
5. Outline the possible complications of severe ethanol poisoning and how these should be managed.

A 34-year-old male was admitted to hospital because of bilateral weakness of the legs beginning 2 days before. He gave a history of being a glue sniffer for at least 10 years but denied abuse of any other drugs or medications. He had previously experienced weakness after glue sniffing. The patient’s pulse was 85 bpm, respiration 18 bpm, blood pressure 162/79 mmHg and temperature was 35.1°C. The patient was alert and oriented. Neurologic examination demonstrated flaccid extremities. The muscle power of the upper and lower extremities was 3/6 and 2/6, respectively.

The serum creatinine was 106 mmol/L, calcium 2.3 mmol/L, glucose 7.2 mmol/L, sodium 135 mmol/L, and potassium 1.5 mmol/L.

Four hours later, this patient developed respiratory distress. The arterial blood gas showed:

pH on FiO₂ 0.2 was 7.038, PaCO₂ 50 mm Hg, HCO₃ 13.2 mmol/L, and PaO₂ 55.2 mm Hg.

Case derived from Kao K, Tsai Y, Lin M, et al. Hypokalaemic Muscular Paralysis Causing Acute Respiratory Failure due to Rhabdomyolysis with Renal Tubular Acidosis in a Chronic Glue Sniffer. J Toxicol Clin Toxicol 2000;38:679–681.

1. What treatment is required?
2. What are the possible causes of the patient’s weakness and respiratory failure?
   Relatives bring in a container of the glue the patient had been sniffing. The main active ingredient seems to be toluene.
3. What other possible complications may occur?