|LETTER TO EDITOR
|Year : 2013 | Volume
| Issue : 3 | Page : 413-414
Intensive care unit psychosis a well known fact but rarely thought early
Vanita Ahuja1, Nitika Goel1, Subhash Das2, Pritam Singh3
1 Department of Anaesthesia and Intensive Care, Government Medical College and Hospital, Chandigarh, India
2 Department of Psychiatry, Government Medical College and Hospital, Chandigarh, India
3 Department of Medicine, Government Medical College and Hospital, Chandigarh, India
|Date of Web Publication||27-Aug-2013|
Department of Anaesthesia and Intensive Care, Government Medical College and Hospital, Chandigarh
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Ahuja V, Goel N, Das S, Singh P. Intensive care unit psychosis a well known fact but rarely thought early. J Anaesthesiol Clin Pharmacol 2013;29:413-4
|How to cite this URL:|
Ahuja V, Goel N, Das S, Singh P. Intensive care unit psychosis a well known fact but rarely thought early. J Anaesthesiol Clin Pharmacol [serial online] 2013 [cited 2021 Jan 22];29:413-4. Available from: https://www.joacp.org/text.asp?2013/29/3/413/117075
Acute organophosphorus poisoning (OPC) is quite prevalent in developing countries.  It often presents as suicidal and at times accidental dermal, respiratory, or oral exposure to pesticides. Acute cholinergic crisis occurs early in these patients due to the involvement of neuromuscular junctions, parasympathetic system, and central nervous system with respiratory failure occurring early or many hours later hence, requiring intensive care unit (ICU) admission.  Patients with OPC suffer from acute cholinergic crisis, intermediate syndrome (IMS), and its related problems. At times, due to several inconsistencies in presentation of ICU psychosis; fluctuating level of consciousness, poor orientation, delusions and hallucinations, and behavioural anomalies, such as aggression or passivity, these may be confused with atypical manifestations of OPC poisoning, IMS and adverse effect of multiple drugs given during ICU stay of a patient hence a delay in managing these patients.
A 14-year-old female presented with complaints of sudden onset of breathlessness and altered sensorium. The past history did not reveal any other comorbid illness. She was diagnosed as a case of accidental OPC poisoning. Trachea was intubated and intravenous (IV) atropine 5 mg/hr and IV pralidoxime (PAM) 1g 8 hourly was started. Patient was shifted to ICU and her respiration was supported with mechanical ventilation. Her baseline routine investigations were acceptable. IV atropine was stopped after appearance of signs of complete atropinization (32-35 hours after start). IV PAM was continued up till 5 days. Patient was gradually weaned from ventilator support but required heavy sedation with IV morphine 2 mg/hr, IV midazolam 2 mg/hr, IV diazepam 10 mg BD, IV promethazine 25 mg TID, IV haloperidol 2-10 mg as required, trials of IV infusion of propofol, and dexmedetomidine for sedation. Patient was conscious, hemodynamically stable, normal blood investigations, good cough reflex and motor power but was agitated, with excessive sweating and showed constant protrusion of tongue along with difficulty in opening and closing of mouth. Patient received spontaneous breathing trial with acceptable blood gases and hemodynamics. Patient's aggressive behavior was thought to be due to oral intubation. Patient's trachea was extubated but the extubation trial failed due to patient's inability to maintain patent airway with shallow breathing. Patient's agitated behavior increased gradually in with rigidity in both her upper limbs, increased protrusion of tongue and difficulty in opening and closing of mouth and also some features suggestive of catatonia (sudden hyperactivity, rigid posture, mutism). Trachea was reintubated and further ventilation was planned with synchronised intermittent positive pressure ventilation (SIMV). Fibreoptic bronchoscopy revealed no pathology. Patient had one episode of ventilator associated pneumonia and was treated with appropriate antibiotics. A percutaneous dilatational tracheostomy with 7.5-mm ID was done and respiration was supported with mechanical ventilation. Due to technical problems, her serum acetyl cholinesterase report was delayed by 10 days which were slightly below normal 3.69 IU/dl (4.65-12.2 IU/dl). Cerebrospinal fluid (CSF) analysis was done which was completely normal. Respiration was supported with continuous positive pressure ventilation (CPAP) and the blood gas trend were normal with no evidence of hypoxia.
A diagnostic dilemma occurred and psychiatric consultation was sought. Per oral olanzapine 2.5 mg BD and IV lorazepam 1 mg TID were started. All sedative drugs were tapered and promethazine and haloperidol were stopped. Patient's symptoms improved and respiratory support was gradually weaned off from ventilator. Lorazepam was tapered and stopped over 1 week. Dose of olanzapine was gradually reduced to 2.5 mg HS and thereafter stopped after 10 days. Patient's trachea was decannulated and patient was discharged from ICU after complete recovery. Patient was discharged home after 1 week in ward and now patient is healthy.
OPC poisioning is poisoning is the quite common in Southeast Asia due to its easy availability.  Due to no validated scoring systems for categorizing severity or predicting outcome of acute organophosphorus poisoning complete recovery on clinical judgment is difficult.
Initial resuscitation with PAM, atropine and oxygen is considered the mainstays of treatment of OPC poisoning. Atropine boluses are given initially in dose of 0.6-3 mg followed by infusion at dose sufficient to maintain cardiovascular and respiratory stability and prevent toxicity. , Initially atropine psychosis was suspected in this patient due to restless requiring heavy sedation. In atropine psychosis, patients become agitated and pyrexia occurs by third day after discontinuing atropine infusion, with absent bowel sounds and urinary retention.  Other symptoms were not present in our patient except agitation which did not improve even 5 days after stopping atropine infusion. The diagnosis of atropine psychosis was now ruled out and intermediate syndrome was considered.
IMS develops 12-96 hrs after exposure and reflects prolonged action of acetylcholine at nicotinic receptors due to release of fat-soluble organophosphorus from fat stores. Such crisis can occur for several days to weeks after ingestion of some organophosphorus compounds. The clinical features are weakness in ocular, bulbar, neck, proximal limb and respiratory muscles with occasional dystonic posturing, requiring mechanical ventilation in an ICU for several days.  Treatment is mainly supportive and complete recovery occurs in 5-18 days. The tidal volume was checked every 4 h and no value was less than 5 mL/kg. Our patient was conscious with no signs of muscle weakness or peripheral respiratory failure and fulfilled criteria for extubation with normal arterial blood gases. The diagnosis of IMS was also now ruled out.
Patient's agitation increased in spite of multiple drugs. Psychiatric consultation was sought and now ICU psychosis was considered. Sweating in this patient could have occurred as result of physical restraint used for agitated patients in ICU and atropine as it inhibits normal thermoregulatory responses. Adequate sedation is therefore important. The features of ICU psychosis occurs rapidly include fluctuating level of consciousness, poor orientation, delusions and hallucinations, and behavioral anomalies, such as aggression and/or passivity. , In addition to physiological causes other causes including metabolic disturbances, electrolyte imbalances, withdrawal syndromes, acute infection (intracranial and systemic), seizures, head trauma, vascular disorders, and intracranial space-occupying lesions were ruled out in our patient. Drugs that are commonly used in ICU including propofol, morphine sulfate, anticholinergics, H1 and H2 antagonists could have contributed to ICU psychosis in our patient.  Other factors causing ICU psychosis include psychological stressors, sleep deprivation, noise, adequate fluid and electrolyte balance, nutrition and vitamin supply were taken care of in our patient.  Haloperidol, 0.5-2.0 mg, 1 to 4 times daily, has been accepted as the treatment of choice.  But in our patient, the use of haloperidol resulted in extra-pyramidal symptoms - rigidity in both upper limb and lower limbs and oromandibular dystonia (difficulty in opening/closing of mouth and protrusion of tongue). Neuroleptic malignant syndrome (NMS) is a life-threatening neurological emergency associated with the use of neuroleptic agents with the "typical" high potency agents (e.g., haloperidol, fluphenazine). Central dopamine receptor blockade in the hypothalamus causes hyperthermia and other signs of dysautonomia and nigrostriatal dopamine pathways leads to rigidity and tremor.  The other diagnosis that present similar to NMS are serotonin syndrome, malignant hyperthermia, malignant catatonia, and other drug-related syndromes. The trends of creatine phospho kinase levels were normal in this patient and there were no episodes of hyperthermia except during VAP and hence a clinical diagnosis of NMS was unlikely. Haloperidol was replaced by newer antipsychotic olanzapine which has similar affects on delirium in ICU patients with fewer adverse events.  Following the start of olanzapine, patient's symptoms resolved with complete neurological recovery.
Management of patient with OPC poisoning depends upon medical management and ICU care. Use of multiple drugs and physical restrain would have caused ICU psychosis in our patient, complicating the primary diagnosis of OPC.
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