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Review Article
Pharmacology Predictors of intermediate syndrome after organophosphorus poisoning and its management in Nepal
Acute and Critical Care 2026;41(2):262-269.
DOI: https://doi.org/10.4266/acc.002825
Published online: April 17, 2026

Department of Critical Care Medicine, Nepal Mediciti, Lalitpur, Nepal

Corresponding author: Saroj Poudel Department of Critical Care Medicine, Nepal Mediciti, Bhaisepati, Lalitpur 44700, Nepal Tel: +977-98-6498-8941 Email: itsmesarozz@gmail.com
• Received: July 17, 2025   • Revised: October 26, 2025   • Accepted: November 2, 2025

© 2026 The Korean Society of Critical Care Medicine

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

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  • Organophosphorus (OP) poisoning is a global public health challenge, is common in agricultural regions, and is associated with high morbidity and mortality. Intermediate syndrome (IMS) is a delayed complication of OP poisoning that usually occurs 24–96 hours post-exposure and is characterized by proximal muscle weakness, cranial nerve palsies, and respiratory failure. The syndrome significantly increases mortality if not identified and managed promptly. This review comprehensively examines the predictors of IMS, including clinical, biochemical, and electrophysiological markers, and evaluates current management strategies. The key predictors are severe initial poisoning, low initial acetylcholinesterase level, and specific electrophysiological abnormalities. Management involves early recognition, antidote administration (atropine and oximes), respiratory support, and emerging therapies like magnesium sulfate. Challenges such as diagnostic uncertainty and resource constraints in low-income settings are discussed, alongside future directions for research and prevention. Understanding these predictors and optimizing management protocols are critical to improving outcomes in IMS following OP poisoning.
  • Key Words: intensive care unit; organophosphate poisoning; respiratory insufficiency
Organophosphorus (OP) compounds, widely used as pesticides and occasionally as chemical weapons, are a leading cause of poisoning in developing countries, with an estimated 200,000 deaths annually [1]. These compounds inhibit acetylcholinesterase (AChE), leading to acetylcholine accumulation, which manifests as acute cholinergic crisis with muscarinic, nicotinic, and central nervous system symptoms collectively known as intermediate syndrome (IMS). While acute management with atropine and oximes is well-established, the pathophysiology and management of IMS remain poorly understood. This syndrome first was described by Senanayake and Karalliedde [2] in 1987. IMS typically emerges 24–96 hours after acute poisoning, following resolution of cholinergic symptoms but before the onset of delayed neuropathy. It is characterized by proximal muscle weakness, cranial nerve palsies, and respiratory muscle paralysis, which can lead to ventilatory failure and death if not managed promptly. The syndrome occurs in approximately 20% of patients following oral exposure to OP pesticides. The incidence varies geographically: studies from South Asia report higher rates up to 65% compared with developed regions (15%–20%) [3-7]. Mortality rate ranges from 10% to 20% depending on the compound, time to presentation, and adequacy of critical care [8,9].
IMS poses a significant challenge due to its unpredictable onset and variable presentation, complicating timely diagnosis and intervention. The syndrome is particularly prevalent in regions with high pesticide use, where access to intensive care and diagnostic tools is often limited. Understanding the clinical, biochemical, and electrophysiological predictors of IMS is essential for identifying at-risk patients early. This review analyzes the current evidence on the predictors of IMS and the management approaches, highlighting challenges and future directions to reduce the burden of this devastating complication.
There are several factors that indicate the possibility of development of IMS after OP poisoning (Table 1). These factors can be divided into clinical, biochemical, and electrophysiological factors as below.
Clinical Predictors
Development of IMS is closely linked to the severity and characteristics of the initial OP poisoning. Severe acute cholinergic symptoms, such as profound muscle fasciculations, seizures, or coma, are strongly associated with IMS risk. The World Health Organization classifies OP compounds by toxicity, with class I agents (e.g., parathion, monocrotophos) posing the highest risk due to their potent AChE inhibition [10]. Studies have shown that patients requiring high doses of atropine or prolonged mechanical ventilation in the acute phase are more likely to develop IMS, likely due to sustained acetylcholine overload [11].
Delayed or inadequate antidote administration significantly increases IMS risk. For instance, failure to administer pralidoxime within 24–48 hours of exposure can lead to persistent AChE inhibition, a key precursor to IMS [12]. Prolonged exposure, such as through large-dose ingestion or dermal contact in occupational settings, also heightens risk by maintaining high OP levels in the body [13]. Specific OP compounds, particularly lipophilic agents like fenthion and dimethoate, are more frequently implicated in IMS due to their slow metabolism and prolonged AChE inhibition [14]. These compounds form stable complexes with AChE, delaying recovery and increasing the likelihood of neuromuscular complications.
Biochemical Predictors
Biochemical markers play a critical role in predicting IMS. Low red blood cell (RBC) AChE activity, typically below 10%–20% of normal at presentation, is a strong predictor of IMS [15]. Persistent AChE inhibition beyond 24 hours, often due to inadequate oxime therapy, further elevates risk [16]. Elevated serum creatine kinase levels, indicative of muscle damage, is common in IMS patients, reflecting myotoxicity from prolonged nicotinic receptor stimulation [17]. Low serum cholinesterase levels also correlate with IMS, serving as an accessible biomarker in resource-limited settings [18].
Electrolyte imbalances, particularly hypokalemia and hypomagnesemia, exacerbate neuromuscular dysfunction and are frequently reported in severe OP poisoning [19]. These imbalances can disrupt muscle membrane stability, contributing to weakness. Additionally, emerging research suggests that oxidative stress markers, such as elevated malondialdehyde levels, can predict IMS by indicating cellular damage from OP exposure [20]. Regular monitoring of these biochemical parameters in the first 48 hours post-poisoning can aid in risk stratification and guide therapeutic decisions.
Electrophysiological Predictors
Electrophysiological studies provide valuable insights into IMS risk. Repetitive compound muscle action potentials following a single stimulus on nerve conduction studies indicate prolonged neuromuscular junction dysfunction, a hallmark of IMS [21]. A decremental response on repetitive nerve stimulation (RNS) at low frequencies (3–5 Hz) is a reliable early indicator of the syndrome, often detectable before clinical symptoms [22]. Single-fiber electromyography reveals increased jitter and blockage, reflecting impaired neuromuscular transmission, and is particularly useful in high-risk patients [4]. Early identification of these electrophysiological abnormalities allow clinicians to anticipate IMS and initiate preventive measures. However, access to such diagnostic tools is often limited in low-resource settings, underscoring the need for portable, cost-effective alternatives.
Patient-Related Factors
Patient-specific factors influence IMS susceptibility. Elderly patients or those with pre-existing neuromuscular disorders are at higher risk due to reduced physiological reserve [23]. Malnutrition, prevalent in rural populations where use of OP pesticides is common, exacerbates muscle weakness and delays recovery [24]. Additionally, genetic variations in enzymes like paraoxonase-1, which detoxify OP compounds, can modulate IMS risk, though evidence remains preliminary [25]. These factors highlight the importance of a holistic approach to risk assessment, considering both environmental and patient-specific variables.
IMS is primarily driven by prolonged AChE inhibition at the neuromuscular junction, leading to nicotinic receptor desensitization and muscle weakness [18]. This sustained inhibition results from the formation of stable OP-AChE complexes, particularly with lipophilic compounds, which resist reactivation by oximes [26]. Oxidative stress, triggered by OP-induced reactive oxygen species, exacerbates neuronal and muscular damage, contributing to IMS [13]. Excitotoxicity from excessive acetylcholine stimulation also can cause secondary neuronal injury, while direct myotoxicity from certain OPs (e.g., fenthion) further impairs muscle function [14]. The delayed onset of IMS, typically 24–96 hours post-exposure, suggests a combination of persistent OP metabolism, inadequate AChE reactivation, and cumulative neuromuscular damage. Understanding this pathophysiology is crucial for developing targeted therapies and identifying early interventions to prevent IMS progression.
Early Recognition and Monitoring
Early recognition of IMS is critical to prevent fatal outcomes. Patients with severe OP poisoning should be monitored in an intensive care unit (ICU) for 72–96 hours for signs of IMS, such as neck flexor weakness, cranial nerve palsies, or respiratory distress [27]. Regular clinical assessments, including muscle strength testing, are essential. Electrophysiological monitoring, particularly RNS and nerve conduction studies, can detect subclinical neuromuscular dysfunction, enabling preemptive intervention [21]. Serial measurement of RBC AChE and serum creatine kinase levels provides additional prognostic value [15,17]. In resource-limited settings, where electrophysiological tools might be unavailable, clinical vigilance and biochemical monitoring are critical for identifying at-risk patients.
Pharmacological Management
Atropine remains the cornerstone of management for acute OP poisoning, targeting muscarinic symptoms but offering limited protection against IMS [1]. An initial loading dose of 1.8–3.6 mg is rapidly administered via intravenous push. If atropinization does not occur within 3–5 minutes, the dose is doubled at that time interval until the patient is fully atropinized. The infusion is maintained at 10%–20% of the total loading dose/hour intravenously, continued until cholinergic signs resolve (typically 24–48 hours), and then tapered as the symptoms improve [28].
Oximes, such as pralidoxime or obidoxime, are critical for reactivating AChE and reducing IMS risk if administered within 24–48 hours. For severe cases, the recommended loading dose is 30 mg/kg of IV pralidoxime over 10–20 minutes, followed by a continuous infusion of 8–10 mg/kg per hour until clinical recovery. However, the efficacy of this treatment is lower for lipophilic OPs [29]. Once IMS develops, atropine is not needed unless cholinergic symptoms recur due to ongoing absorption or re-distribution. Oxime therapy is not associated with improved survival once IMS develops, and continued oxime use can prolong neuromuscular weakness [4].
Adjunctive therapies, such as magnesium sulfate, administered as 4 g IV over 24 hours, show promise in stabilizing neuromuscular junctions and reducing excitotoxicity, with clinical trials reporting improved outcomes [30]. Supportive therapies, including correction of hypokalemia and hypomagnesemia, are essential to prevent exacerbation of muscle weakness [19]. Nutritional support, particularly in malnourished patients, aids recovery and reduces complications [24].
Respiratory Support
Respiratory failure is the leading cause of death in IMS and requires prompt intervention. Non-invasive ventilation can be effective in patients with early respiratory compromise, delaying or preventing intubation [31]. However, severe IMS often requires intubation and mechanical ventilation, with weaning guided by clinical and electrophysiological recovery [32]. Short-acting or intermediate-acting non-depolarizing agents, such as vecuronium or atracurium, should be used to facilitate intubation and mechanical ventilation. Succinylcholine should be avoided due to unpredictable response from low plasma cholinesterase activity. The lowest effective doses should be used and titrated by train-of-four monitoring to prevent prolonged weakness. Close monitoring of respiratory muscle strength and arterial blood gases is critical to optimize ventilatory support. In resource-constrained settings, where ventilators are scarce, prioritizing early non-invasive ventilation and manual ventilation strategies can be lifesaving.
Emerging Therapies
Emerging therapies show potential in IMS management. Antioxidants, such as N-acetylcysteine or vitamin C, can mitigate oxidative stress and reduce IMS severity, though evidence is preliminary [20]. Neuromuscular junction stabilizers, like 3,4-diaminopyridine, are under investigation for enhancing neuromuscular transmission, but robust clinical data are lacking [33]. Research into novel AChE reactivators, designed to target lipophilic OPs, is ongoing and could lead to improvement in outcomes [34].
Long-Term Management and Prevention
Post-IMS recovery requires physical therapy to restore muscle strength and prevent contractures [4]. Education on safe pesticide use, including personal protective equipment, is essential to prevent recurrent exposures, particularly in agricultural communities [35]. Public health campaigns and regulatory measures to restrict highly toxic OP compounds can further reduce IMS incidence. Long-term follow-up is necessary to monitor delayed neuropathy and other sequelae.
Despite advances, IMS management faces significant challenges. The lack of standardized diagnostic criteria complicates early recognition, and there is need for a unified scoring system integrating clinical, biochemical, and electrophysiological markers [18]. The variable efficacy of oximes, particularly for lipophilic OPs, highlights the need for novel AChE reactivators [33]. Resource constraints in low-income settings, where OP poisoning is most prevalent, limit access to ICU care, ventilators, and electrophysiological diagnostics, underscoring the need for cost-effective solutions [27]. Future research should focus on developing rapid, portable diagnostic tools, such as point-of-care AChE assays, and novel therapeutics targeting oxidative stress and neuromuscular dysfunction. Public health interventions, including pesticide regulation and farmer education, are critical to reducing IMS incidence. Collaborative global efforts are needed to address these challenges and improve outcomes in OP poisoning.
IMS is a life-threatening complication of OP poisoning, with predictors including severe initial symptoms, low AChE levels, and electrophysiological abnormalities. Effective management relies on early recognition, timely antidote administration, and robust supportive care, particularly respiratory support (Table 2). Emerging therapies and preventive strategies offer hope, but challenges like diagnostic uncertainty and resource limitations persist. Advances in diagnostics, novel therapeutics, and public health measures are essential to mitigate the burden of IMS, particularly in high-risk regions. Continued research and global collaboration will be key to improving outcomes and reducing the impact of this devastating syndrome.
▪ Intermediate syndrome (IMS) is a serious complication of organophosphorus poisoning, occurring 24–96 hours post-exposure, with manifestations including muscle weakness and respiratory failure.
▪ Several factors, such as severe presenting symptoms or low serum acetylcholinesterase activity, and patient-related factors like age assist in identifying individuals at risk for IMS.
▪ Successful management includes early recognition, treatment like atropine and oximes, and respiratory support.

CONFLICT OF INTEREST

No potential conflict of interest relevant to this article was reported.

FUNDING

None.

ACKNOWLEDGMENTS

We would like to thank the members of our department of critical care, whose work on organophosphorus poisoning and intermediate syndrome has formed the base of this review.

AUTHOR CONTRIBUTIONS

Conceptualization: KK. Methodology: KK, SP. Formal analysis: KK. Data curation: KK, SP. Visualization: KK, SP. Project administration: KK. Writing – original draft: KK, SP. Writing – review & editing: KK, SP. All authors read and agreed to the published version of the manuscript.

acc-002825f1.jpg
Table 1.
Summary of predictors of Intermediate syndrome after OP poisoning
Category Predictor Description/details Associated risk
Clinical risk factor Severity of acute poisoning Severe initial cholinergic symptoms (e.g., profound fasciculations, seizures, coma). WHO class I OPs (e.g., parathion) pose higher risk. High risk due to profound AChE inhibition and sustained acetylcholine overload
Delayed or inadequate treatment Late or insufficient administration of antidotes (e.g., atropine, pralidoxime) within 24–48 hr Increased risk due to persistent AChE inhibition
Prolonged exposure High-dose ingestion or prolonged dermal exposure to OP compounds Elevates risk by maintaining high OP levels in the body
Specific OP compounds Lipophilic OPs (e.g., fenthion, dimethoate, monocrotophos) with slow metabolism Higher risk due to prolonged AChE inhibition
Biochemical predictor Low AChE levels RBC AChE activity <10%–20% of normal at presentation; persistent inhibition beyond 24 hours Strong predictor of IMS due to sustained neuromuscular junction dysfunction
Elevated serum CK High CK levels indicating muscle damage from prolonged nicotinic receptor stimulation Correlates with IMS due to myotoxicity
Low serum cholinesterase Reduced serum cholinesterase levels as a marker of OP toxicity Accessible biomarker associated with IMS risk
Electrolyte imbalances Hypokalemia and hypomagnesemia disrupting muscle membrane stability Exacerbates neuromuscular dysfunction, increasing IMS risk
Oxidative stress markers Elevated malondialdehyde levels indicating cellular damage from OP exposure Emerging predictor of IMS related to oxidative stress
Electrophysiological predictor Repetitive firing on nerve conduction studies Repetitive compound muscle action potentials following a single stimulus Indicates prolonged neuromuscular junction dysfunction, a hallmark of IMS
Decremental response on RNS Decremental response at low frequencies (3–5 Hz) on RNS, detectable before clinical symptoms. Reliable early indicator of IMS risk
SFEMG abnormalities Increased jitter and blocking on SFEMG, reflecting impaired neuromuscular transmission Useful for early detection of IMS in high-risk patients

OP: organophosphorus; WHO: World Health Organization; OP: organophosphorus; AChE: acetylcholinesterase; RBC: red blood cell; IMS: intermediate syndrome; CK: creatine kinase; RNS: repetitive nerve stimulation; SFEMG: single fiber electromyography.

Table 2.
Management strategies for Intermediate Syndrome
Category Strategy Description/details Key consideration
Early recognition and monitoring ICU monitoring Patients with severe OP poisoning should be monitored in ICU for 72–96 hours for early signs of neck flexor weakness, cranial nerve palsies, or respiratory distress. Essential for preemptive intervention; clinical vigilance is required in limited-resource settings if electrophysiological monitoring in not possible.
Include regular clinical assessments (e.g., muscle strength testing) and serial RBC AChE/CK measurements Electrophysiological monitoring (e.g., RNS) can help detect subclinical issues early.
Pharmacological management Atropine administration Cornerstone for muscarinic symptoms; high doses may be needed in severe cases. Limited protection against IMS; primarily for acute phase: monitor for atropine toxicity (e.g., delirium, hyperthermia).
Oximes (e.g., pralidoxime or obidoxime) Reactivate AChE; administration within 24–48 hours after OP exposure is preferable. Administer as continuous infusion (e.g., pralidoxime 500 mg/hr in severe cases). Reduced efficacy for lipophilic OPs; critical timing to prevent persistent inhibition of AChE
Magnesium sulfate Administer 4 g IV over 24 hours to help stabilize the neuromuscular junctions and decreased excitotoxicity Promising in trials for improved outcomes; addresses electrolyte imbalances like hypomagnesemia
Supportive therapies Correct electrolyte imbalances (e.g., hypokalemia, hypomagnesemia) and provide nutritional support for malnourished patients Prevents exacerbation of weakness; especially important in rural or low-resource settings
Respiratory support Non-invasive ventilation Indicated for early respiratory compromise to delay or avoid intubation Effective in mild cases; and assess respiratory muscle strength and arterial blood gases
Intubation and mechanical ventilation Indicated for severe IMS with ventilatory failure; potential to wean as patient recovers clinically and electrophysiologically Leading cause of death if delayed; prioritize in resource-scarce settings with manual means if ventilators are limited
Emerging therapies Antioxidants (e.g., N-acetylcysteine or vitamin C) May reduce oxidative stress; may reduce severity of IMS Preliminary evidence; yet to undergo further trials
Neuromuscular junction stabilizers (e.g., 3,4-diaminopyridine) May improve neuromuscular transmission Generalized research with a lack of clinical data or evidence base
Long-term management and prevention Physical therapy Muscle strength recovery, preventing contractures following IMS Necessary for recovery; monitor for delayed neuropathy
Education and prevention Promote safe agricultural pesticide use (e.g., personal protective equipment); public health campaigns and regulation of toxic OPs Reduces incident occurrences in agricultural areas, especially in high-risk regions

ICU: intensive care unit; OP: organophosphorus; RBC: red blood cell; AChE: acetylcholinesterase; CK: creatine kinase; RNS: repetitive nerve stimulation; IMS: intermediate syndrome; IV: intravenous.

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        Predictors of intermediate syndrome after organophosphorus poisoning and its management in Nepal
        Acute Crit Care. 2026;41(2):262-269.   Published online April 17, 2026
        DOI: https://doi.org/10.4266/acc.002825
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      Predictors of intermediate syndrome after organophosphorus poisoning and its management in Nepal
      Category Predictor Description/details Associated risk
      Clinical risk factor Severity of acute poisoning Severe initial cholinergic symptoms (e.g., profound fasciculations, seizures, coma). WHO class I OPs (e.g., parathion) pose higher risk. High risk due to profound AChE inhibition and sustained acetylcholine overload
      Delayed or inadequate treatment Late or insufficient administration of antidotes (e.g., atropine, pralidoxime) within 24–48 hr Increased risk due to persistent AChE inhibition
      Prolonged exposure High-dose ingestion or prolonged dermal exposure to OP compounds Elevates risk by maintaining high OP levels in the body
      Specific OP compounds Lipophilic OPs (e.g., fenthion, dimethoate, monocrotophos) with slow metabolism Higher risk due to prolonged AChE inhibition
      Biochemical predictor Low AChE levels RBC AChE activity <10%–20% of normal at presentation; persistent inhibition beyond 24 hours Strong predictor of IMS due to sustained neuromuscular junction dysfunction
      Elevated serum CK High CK levels indicating muscle damage from prolonged nicotinic receptor stimulation Correlates with IMS due to myotoxicity
      Low serum cholinesterase Reduced serum cholinesterase levels as a marker of OP toxicity Accessible biomarker associated with IMS risk
      Electrolyte imbalances Hypokalemia and hypomagnesemia disrupting muscle membrane stability Exacerbates neuromuscular dysfunction, increasing IMS risk
      Oxidative stress markers Elevated malondialdehyde levels indicating cellular damage from OP exposure Emerging predictor of IMS related to oxidative stress
      Electrophysiological predictor Repetitive firing on nerve conduction studies Repetitive compound muscle action potentials following a single stimulus Indicates prolonged neuromuscular junction dysfunction, a hallmark of IMS
      Decremental response on RNS Decremental response at low frequencies (3–5 Hz) on RNS, detectable before clinical symptoms. Reliable early indicator of IMS risk
      SFEMG abnormalities Increased jitter and blocking on SFEMG, reflecting impaired neuromuscular transmission Useful for early detection of IMS in high-risk patients
      Category Strategy Description/details Key consideration
      Early recognition and monitoring ICU monitoring Patients with severe OP poisoning should be monitored in ICU for 72–96 hours for early signs of neck flexor weakness, cranial nerve palsies, or respiratory distress. Essential for preemptive intervention; clinical vigilance is required in limited-resource settings if electrophysiological monitoring in not possible.
      Include regular clinical assessments (e.g., muscle strength testing) and serial RBC AChE/CK measurements Electrophysiological monitoring (e.g., RNS) can help detect subclinical issues early.
      Pharmacological management Atropine administration Cornerstone for muscarinic symptoms; high doses may be needed in severe cases. Limited protection against IMS; primarily for acute phase: monitor for atropine toxicity (e.g., delirium, hyperthermia).
      Oximes (e.g., pralidoxime or obidoxime) Reactivate AChE; administration within 24–48 hours after OP exposure is preferable. Administer as continuous infusion (e.g., pralidoxime 500 mg/hr in severe cases). Reduced efficacy for lipophilic OPs; critical timing to prevent persistent inhibition of AChE
      Magnesium sulfate Administer 4 g IV over 24 hours to help stabilize the neuromuscular junctions and decreased excitotoxicity Promising in trials for improved outcomes; addresses electrolyte imbalances like hypomagnesemia
      Supportive therapies Correct electrolyte imbalances (e.g., hypokalemia, hypomagnesemia) and provide nutritional support for malnourished patients Prevents exacerbation of weakness; especially important in rural or low-resource settings
      Respiratory support Non-invasive ventilation Indicated for early respiratory compromise to delay or avoid intubation Effective in mild cases; and assess respiratory muscle strength and arterial blood gases
      Intubation and mechanical ventilation Indicated for severe IMS with ventilatory failure; potential to wean as patient recovers clinically and electrophysiologically Leading cause of death if delayed; prioritize in resource-scarce settings with manual means if ventilators are limited
      Emerging therapies Antioxidants (e.g., N-acetylcysteine or vitamin C) May reduce oxidative stress; may reduce severity of IMS Preliminary evidence; yet to undergo further trials
      Neuromuscular junction stabilizers (e.g., 3,4-diaminopyridine) May improve neuromuscular transmission Generalized research with a lack of clinical data or evidence base
      Long-term management and prevention Physical therapy Muscle strength recovery, preventing contractures following IMS Necessary for recovery; monitor for delayed neuropathy
      Education and prevention Promote safe agricultural pesticide use (e.g., personal protective equipment); public health campaigns and regulation of toxic OPs Reduces incident occurrences in agricultural areas, especially in high-risk regions
      Table 1. Summary of predictors of Intermediate syndrome after OP poisoning

      OP: organophosphorus; WHO: World Health Organization; OP: organophosphorus; AChE: acetylcholinesterase; RBC: red blood cell; IMS: intermediate syndrome; CK: creatine kinase; RNS: repetitive nerve stimulation; SFEMG: single fiber electromyography.

      Table 2. Management strategies for Intermediate Syndrome

      ICU: intensive care unit; OP: organophosphorus; RBC: red blood cell; AChE: acetylcholinesterase; CK: creatine kinase; RNS: repetitive nerve stimulation; IMS: intermediate syndrome; IV: intravenous.

      Table 1.

      Table 2.

      ACC : Acute and Critical Care
      © The Korean Society of Critical Care Medicine.
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