Erratum: Respiratory Complications of Organophosphorus Nerve Agent and Insecticide Poisoning. Implications for Respiratory and Critical Care

The authors of the article by Hulse and colleagues (1), published in the December 15, 2014, issue of the Journal, would like to correct several errors. In the Figure 3 legend (p. 1345), the phrase “48 hours after administration of saline into the lung” in the second sentence should be corrected to read “48 hours after sham bronchoscopy and saline BAL (at 24 and 48 h).” The words “of the same lungs” appearing in the sixth and eighth sentences should be replaced by the words “similarly affected lungs.” The corrected figure legend should read:

Figure 3. Effects of hematogenous organophosphorus (OP) and aspirated OP on minipig lung. Comparison of lung architecture in anesthetized minipigs 48 hours after sham bronchoscopy and saline BAL (at 24 and 48 h) (control pig; A, D, and G), gastric contents and the agricultural OP insecticide dimethoate EC40 into the contralateral lung (indirect hematogenous injury; B, E, and H), and gastric contents and agricultural OP insecticide dimethoate EC40 into the right lung (direct injury; C, F, I). (A–C) Light microscopy images (original magnification: ×10–20) with hematoxylin and eosin. Compared with indirect injury, direct injury caused greater alveolar and interstitial edema, neutrophil infiltration, hemorrhage, fibrin deposition, vascular congestion, and necrosis. Images edited in PowerPoint. (D–F) Scanning electron microscopy images (original magnification: ×171–324) of similarly affected lungs. Direct injury shows extensive destruction of the alveolar capillary framework, with fibrin mesh and clot formation. (G–I) Transmission electron microscopy images (original magnification: ×25,000) of similarly affected lungs. Both indirect and direct injury cause alveolar capillary membrane swelling. The black arrow signifies the alveolar capillary membrane in control (G) and indirect (H) lungs. After direct injury, this has led to the alveolar epithelium peeling away into the alveolar space and fibrin deposition (red arrow) in and around the alveolar capillary membrane.

In Table 2 (p. 1349), first paragraph in the comments column, the words “acetylcholinesterase inhibition” should be replaced by “butyrylcholinesterase inhibition.” In the eighth paragraph of the comments column, the second sentence should read: “Note: effects of drugs that are metabolized by either butyrylcholinesterase or esterases may be prolonged in OP poisoning.”

Table 2.

Clinical Management of Organophosphorus-poisoned Patients

Intervention	Comment	Time Point
Maintain airway and provide adequate oxygenation (>85% saturations)	Quick and efficient securing of the airway. Note: the depolarizing neuromuscular blocker suxamethonium will have a prolonged effect (up to 12 h) due to butyrylcholinesterase inhibition. Avoid where possible (25, 112, 113).	Within minutes after nerve agent poisoning, within minutes to hours after insecticide poisoning to avoid hypoxic brain damage
Administer escalating dose atropine regimen	Give intravenous atropine (initially 0.6–3 mg, doubling every 5 min until muscarinic features start to subside). This will help maintain patient oxygenation and lessen the risk of aspiration injury. Infusions of atropine may be required for many days; titrate to effect (93, 94). Do not delay if oxygen is not immediately available (92).	Within minutes after nerve agent poisoning, within minutes to hours after insecticide poisoning to avoid hypoxic brain damage
Administer benzodiazepines	Give diazepam 10–20 mg or lorazepam 2–4 mg to control seizure activity and agitation, and to sedate intubated patients.	Minutes to hours
Administer oximes	Give 1 g pralidoxime or 250 mg obidoxime, then an infusion. Oximes are not of proven clinical benefit but can be considered in patients presenting early. Patients should be weaned when possible, preferably guided by neurophysiological studies.	Hours to days
Ventilation strategy	Use protective ventilation (6 ml/kg); avoid plateau pressures >30 cm H2O.	For the duration of ICU stay; days to weeks
	Response to NDMRs may be unpredictable (25, 114). Titrate dose to effect. Use of aminosteroid NMBAs (e.g., rocuronium) may provide some protection of nicotinic receptors.	As required for intubation and ventilation.
Cardiovascular instability	Dysrhythmias and severe hypotension can occur in OP poisoning and are treated by standard ICU practices (53). Note: effects of drugs that are metabolized by either butyrylcholinesterase or esterases may be prolonged in OP poisoning.	Hours to days
Prevention of VAP	Provide VAP prevention strategies: sit the patient at 30–45°, consider selective digestive and/or oropharyngeal decontamination (66), start antibiotics (after consultation with a local microbiologist) only if bronchopneumonia or sepsis is suspected (64).	Hours to days
Inhaled β-agonists, anticholinergics	Standard therapy for many critical care units. Observe for tachyarrhythmias when combined with intravenous atropine.	For the duration of ICU stay; days to weeks
Prevention of CIP/CIM	Wean as early as possible from the ventilator to reduce the risk of CIP/CIM.	>7 d to weeks
ICU sedation	Minimal sedation and daily sedation holds as per VAP prevention strategies and staffing levels allow (64). This will allow early identification of the return of consciousness in poisoned patients who can then be weaned from the ventilator.	For the duration of ICU stay; days to weeks
Standard ICU care to improve survival of patients with ARDS	GI ulceration care, nutrition, thrombosis prophylaxis, timely antibiotics for infections, judicious intravenous fluid management and lung protective ventilation strategies (115).	For the duration of ICU stay; days to weeks
Careful observation	Careful observation of patients with OP insecticide poisoning will identify cholinergic features, labored respiratory efforts, and proximal muscle weakness heralding the onset of IMS or delayed cholinergic effects.	Hours to days after poisoning and after extubation
Extubation	Requires several hours of successful spontaneous ventilation and the ability to lift their head off the bed on at least three different time points before a trial of extubation should be attempted (96). If prolonged ventilation is anticipated, consider tracheostomy. Be aware of laryngeal muscle dysfunction.	Hours to days

Definition of abbreviations: ARDS = acute respiratory distress syndrome; BuChE = butyrylcholinesterase; CIP = critical illness polyneuropathy; CIM = critical illness myopathy; GI = gastrointestinal; ICU = intensive care unit; IMS = intermediate syndrome; NDMRs = nondepolarizing muscle relaxants; NMBA = neuromuscular blocking agent; OP = organophosphate; VAP = ventilator-associated pneumonia.

The authors apologize for the errors.