We present a case of critical airway obstruction secondary to a solid tracheal mucus plug in a patient with pneumonia. Following failed conventional mucolysis therapy, nebulised N-acetylcysteine acted as a life-saving mucolytic, and prevented imminent cardiorespiratory arrest. Use of oral N-acetylcysteine as a mucolytic has been long established within respiratory medicine in managing chronic airway disease, but is rarely utilised in critically ill or mechanically ventilated patients due to the lack of comparative studies in literature. A 28-year-old female presented to the emergency department with shortness of breath and a productive cough. She was six weeks post-partum with no past medical history. Initial management for a community acquired pneumonia with type 1 respiratory failure included intensive care admission, antibiotics, fluid therapy and bronchodilators. The patient acutely deteriorated 48 h after admission becoming unresponsive and severely hypoxaemic. Intubation did not achieve ventilation, and subsequent direct bronchoscopy revealed a thick, solid, obstructing tracheal mucus plug, superior to the carina. It was resistant to aspiration despite the use of saline flushes, chest physiotherapy and bronchodilators and the bronchoscope could not pass it. N-acetylcysteine, administered via the bronchoscopic port, caused sufficient mucolysis to enable removal of the thick mucus cast, enabling ventilation and gas exchange. Such resistant mucus plugging is a rare cause of failed ventilation, with limited therapeutic options. Here, the unlicensed and rarely reported use of nebulised N-acetylcysteine was a life-saving mucolytic, allowing removal of the obstructing plug and re-establishing ventilation.
SummaryA 51-year-old man suffered a cardiac arrest after an attempted hanging. Post-arrest assessment revealed the bilateral absence of negative 20 somatosensory evoked potentials (N20 SSEPs) which is suggestive of a poor neurological outcome. Current evidence recommends its use in prognostication. Our patient made a good recovery which brings into question the value of negative 20 somatosensory evoked potentials in prognostication with concomitant neck injuries and swelling. KeywordsAbsence, good outcome, N20, SSEP Case historyA 51-year-old man presented to the Emergency Department following a failed hanging attempt. Prehospital management included cardiopulmonary resuscitation for a pulseless electrical activity rhythm, with a return of output after one cycle. On arrival, he was unconscious with a Glasgow coma scale (GCS) of 3, hypertensive (209/121), hypoxic (saturations of 84% on 15 L oxygen via a non-rebreathe mask), and tachycardic (heart rate 125 beats per minute). Moderate swelling was noted around his neck where the ligature had been.Pupils were 4 mm bilaterally and sluggishly reactive to light. Blood gases showed a lactic acidosis with pH 7.01, pO 2 11.8, pCO 2 6.2, base excess À14 and a lactate of 6.59.Bloods revealed the absence of paracetamol and salicylate levels. No other toxicology was measured. Immediate management consisted of intubation and ventilation due to his low GCS and hypoxia. Computed tomography (CT) imaging of the head and neck was normal. The patient was cooled to 36 C for 24 h post-arrest. On Day 2, he developed generalised tonic clonic seizures whilst on propofol and alfentanil sedation. The seizures appeared to self-resolve after approximately one minute; however an electroencephalogram (EEG) was performed on day 2 which confirmed nonconvulsive status. He was treated with phenytoin and lamotrigine. An EEG done on day 4 showed that the non convulsive status had resolved. He remained cardiovascularly stable throughout his admission and did not require any vasopressors. Renal function was normal throughout and he did not require any support. Daily haematology, biochemistry and blood sugars were within normal limits.Sedation was stopped on Day 3. On Day 5, his GCS remained poor at 4 (Eyes 1, Motor 2, Verbal 1) and so brain magnetic resonance imaging (MRI) and somatosensory evoked potentials (SSEP) investigations were carried out. The MRI was normal. N20 SSEPs conducted on Days 5 and 6 at normothermia were absent bilaterally.N13 SSEPs were also absent bilaterally on both occasions, whereas N9 SSEPs were present.On Day 6, clinical assessment revealed the presence of spontaneous eye opening and bilateral pupillary, and corneal responses. Motor assessment revealed an extensor response to pain. Moderate reduction of the neck swelling was observed.Repeat of the N20 SSEPs on Day 7 showed clear bilateral potentials with normal latency. N13 SSEPs were now also present along with the N9 SSEPs.
A 61-year-old man presented to the emergency department following an intentional overdose of 32 g of amisulpride (therapeutic dose: 50-1,200 mg/day). On arrival, he was unconscious (Glasgow Coma Score 3), had poor respiratory effort, hypotension (blood pressure 90/40 mm Hg) and hypothermia (temperature 32.4°C). An ECG demonstrated sinus rhythm, a heart rate of 90 bpm, with intermittent selfresolving ventricular tachycardia and a prolonged QTc interval (corrected QT time, calculated with Bazett' s formula, of 431 msec). Laboratory results included: Na + 141 mmol/L, Cl -102 mmol/L, K + 3.9 mmol/L and an ionised Ca 2+ of 1.17 mmol/L. Blood gases showed a lactic acidosis with a pH of 7.05, base deficit of -15 mmol/L and a lactate of 12 mmol/L. The initial plasma amisulpride level was found to be 50 mg/L. Immediate treatment consisted of intubation, mechanical ventilation and fluid resuscitation. The patient required vasopressor therapy with noradrenaline at a rate of 0.25 µg/kg/min. Despite receiving 5 litres of Hartmann' s solution and maintaining a central venous pressure of around 12 cm H 2 O, his noradrenaline requirements increased to 0.56 µg/kg/min.He was transferred to the intensive care unit (ICU) where haemodynamic assessment using the LiDCO Rapid © technique demonstrated a low cardiac output. Considered together with lactic acidosis, this suggested low global tissue perfusion. This was treated with dobutamine, while continuous veno-venous haemofiltration (CVVHF) and a simultaneous sodium bicarbonate infusion were initiated to reduce the immediate cardiovascular effects of the low pH. CVVHF was maintained almost continuously, at a dose of 35 mL/kg/h. Accusol 35 (Baxter International Inc.) was used as the buffer solution.The plasma amisulpride level following haemofiltration was higher (59.5 mg/L) than the initial level, suggesting either a haemoconcentration effect or continued absorption.The lactic acidosis resolved over the initial 12 hours, but significant cardiovascular instability was a continuing feature over the next few days. There were four recorded episodes of torsades de pointes, one example of which is shown in Figure 1. One episode required a precordial thump, another direct current shock and others were self-resolving. These episodes resolved following further aggressive therapy, as suggested by TOXBASE, aimed at: • Maintenance of serum potassium, calcium, and magnesium levels at the high end of the normal range • Reduction of the QTc interval by increasing the heart rate above 100 bpm using an isoprenaline infusion. 1 After commencing the isoprenaline infusion, no further episodes of torsades de pointes occurred.The maximum QTc of 725 msec (Figure 2) was recorded at 50 hours post-overdose. It remained elevated at 451 msec in spite of therapy until 190 hours post-overdose.In view of the long-term ventilatory requirements, a tracheostomy was inserted on day eight. The patient was successfully decannulated on day 14 and made an uneventful and complete recovery.A 61-year-old man took an amisulprid...
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