Department of Internal Medicine, Postgraduate Institute of Medical Education & Research, Chandigarh, India *Corresponding Author’s e-mail: bhalla.chd@gmail.com داللة مستويات اجللوكوز يف الدم وتغرياته كعوامل تنبؤ بنتائج املرضى املصابني بتسمم فوسفيد األلومنيوم اأرفند �شارما، برا�شانث بال�شربامينني، كريان جل، اأ�شي�ص بّله abstract: Objectives: This study aimed to assess the prognostic significance of blood glucose levels and blood glucose alterations (i.e. hyper- or hypoglycaemia) among patients with aluminium phosphide (AlP) poisoning. Methods: This prospective observational study was conducted at the Postgraduate Institute of Medical Education & Research, Chandigarh, India, between January 2010 and June 2011. All patients presenting to the emergency department with a definitive history of AlP ingestion or symptoms compatible with AlP poisoning were included in the study. Blood glucose levels were recorded at presentation and every six hours thereafter. Alterations in blood glucose levels and other clinical and laboratory variables were subsequently compared between survivors and non-survivors. Results: A total of 116 patients with AlP poisoning were identified. Of these, 57 patients (49%) survived and 59 patients (51%) died. At presentation, the mean blood glucose levels of survivors and non-survivors were 119.9 ± 35.7 mg/dL and 159.7 ± 92.5 mg/dL, respectively (P <0.001). In comparison to the survivors, non-survivors had significantly higher heart rates, total leukocyte counts, blood glucose level alterations and serum creatinine levels (P <0.050). In addition, systolic blood pressure, Glasgow coma scale scores, arterial blood gas pH and bicarbonate values and duration of hospital stay was significantly lower compared to survivors (P <0.001). However, neither blood glucose levels at admission nor blood glucose alterations correlated independently with mortality in a multivariate analysis. Conclusion: The role of blood glucose level alterations in predicting patient outcomes in AlP poisoning cases remains inconclusive. Further studies with larger sample sizes are required. Keywords: Aluminum Phosphide; Poisoning; Blood Glucose; Hyperglycemia; Hypoglycemia; Mortality; Prognostic Factors; India. امللخ�ص: الهدف: هدفت هذه الدرا�شة اإىل تقييم دللة م�شتويات اجللوكوز يف الدم وتغرياته )زياده اأو نق�شان( كعوامل تنبوؤ بنتائج املر�شى امل�شابني بت�شمم فو�شفيد الألومنيوم. الطريقة: اأجريت هذه الدرا�شة الر�شدية يف معهد الدرا�شات العليا للتعليم الطبي والبحوث يف �شانديغار، الهند، يف الوقت بني يناير 2010 و يونيو 2011 على جميع املر�شى القادمني اإىل ق�شم الطوارئ بعد التاأكد من ابتالع فو�شفيد الألومنيوم اأو لديهم اأعرا�ص متوافقة مع هذا الت�شمم. مت ت�شجيل م�شتويات اجللوكوز يف الدم عند قدومهم وكل �شت �شاعات بعد ذلك. متت بعد ذلك مقارنة التغيريات يف م�شتويات اجللوكوز يف الدم وغريها من املتغريات ال�رسيرية واملخربية بني الناجني وغري الناجني من الت�شمم. النتائج: مت حتديد جمموعه 116 مري�شا اأ�شيبو بت�شمم فو�شفيد الألومنيوم. من هوؤلء، جنا 57 مري�شا )%49( وتويف 59 مري�شا )%51(. عند القدوم اإىل ق�شم الطواريء، كان متو�شط م�شتويات ال�شكر يف الدم للناجني وغري الناجني 35.7 ± 119.9 ملغ/دي�شيلرت و 92.5 ± 159.7 ملغم/دي�شيلرت ، على التوايل )P >0.001(. كان لدى غري الناجني باملقارنة مع الناجني قيم اأعلى ب�شكل ملحوظ ملعدل �رسبات قلب، اأعداد كريات الدم البي�ص، تغريات م�شتوى اجللوكوز وم�شتويات الكرياتينني يف الدم )P >0.050(. بالإ�شافة اإىل ذلك، كان �شغط الدم النقبا�شي ومقيا�ص غيبوبة .)P >0.001( غال�شكو ودرجة احلمو�شة وم�شتوى البيكربونات يف الدم ال�رسياين ومدة الإقامة يف امل�شت�شفى اأقل بكثري مقارنة بالناجني ومع ذلك، ل ترتبط م�شتويات اجللوكوز يف الدم عند القدوم ول تغريات اجللوكوز يف الدم ب�شكل م�شتقل مع معدل الوفيات يف التحليل متعدد املتغريات. اخلال�صة: ل يزال دور تغريات م�شتوى اجللوكوز يف الدم يف التنبوؤ بنتائج املر�شى يف حالت ت�شمم فو�شفيد الألومنيوم غري حا�شم. مطلوب مزيد من الدرا�شات مع اأحجام عينة اأكرب. الكلمات املفتاحية: ت�شمم فو�شفيد الألومنيوم؛ جلوكوز الدم؛ ارتفاع ال�شكر يف الدم؛ نق�ص ال�شكر يف الدم؛ معدل الوفيات؛ عوامل التنبوؤ؛ الهند. Prognostic Significance of Blood Glucose Levels and Alterations Among Patients with Aluminium Phosphide Poisoning Arvind Sharma, Prasanth Balasubramanian, Kiran D. Gill, *Ashish Bhalla clinical & basic research Sultan Qaboos University Med J, August 2018, Vol. 18, Iss. 3, pp. e299–303, Epub. 19 Dec 18 Submitted 5 Mar 18 Revisions Req. 10 Apr & 28 May 18; Revisions Recd. 10 May & 5 Jun 18 Accepted 7 Jun 18 Advances in Knowledge - Elevated blood glucose levels have been previously identified as an indicator of poor prognosis in cases of aluminium phosphide (AlP) poisoning. However, the current study found that blood glucose level alterations—namely, hyper- or hypoglycaemia—were not associated with mortality in AlP cases. Application to Patient Care - Based on the findings of the current study, blood glucose level alterations should not be considered predictors of poor patient prognosis in AlP poisoning cases. Patients should therefore be assessed based on a range of clinical and laboratory parameters. doi: 10.18295/squmj.2018.18.03.006 Prognostic Significance of Blood Glucose Levels and Alterations Among Patients with Aluminium Phosphide Poisoning e300 | SQU Medical Journal, August 2018, Volume 18, Issue 3 In India, aluminium phosphide (alp) is the most commonly encountered poison after anti-cholinesterase.1 As a pesticide, AlP is used exten- sively to protect stored products and crops and is available in the form of pellets, tablets or compressed discs. In northern India, an epidemic of AlP poisoning was reported in 1988 in which 285 cases of AlP ingestion were documented, most of which were intentional/ suicidal.2 Although the toxicokinetic properties of AlP are poorly understood, its toxicodynamic properties are exerted by phosphine (PH3), which is released in the stomach when it comes into contact with moisture or hydrochloric acid and results in the inhibition of cytochrome C oxidase and a release of free oxygen radicals, causing oxidative stress.3,4 After oral ingestion, PH3 is quickly absorbed into the body, resulting in systemic toxicity, with death usually resulting from cardiovascular dysfunction.5 Phosphides may also be absorbed in their unhydrolysed salt form.6 Apart from a definitive history of ingestion, a diag- nosis of AlP poisoning can be established by the odour of the patient’s breath, which often smells of garlic or decaying fish, although the former symptom is also seen in calcium carbide poisoning cases.7–9 Other early symptoms include nausea, vomiting, epigastric and retro- sternal pain, anxiety, agitation and dyspnoea.7 In addition, the diagnosis can also be made by silver nitrate testing of the gastric fluid or breath.9 Peripheral circulatory failure and shock are early signs indicating fatal tox- icity.7 The mortality rate in AlP poisoning cases varies from 30–100% and depends upon the dose and freshness of the poison, the onset of clinical manifestations, time until presentation, duration and severity of shock, time until vomiting and treatment modality. The main compl- ications observed in fatal AlP poisoning cases are cardiac dysrhythmias, severe metabolic acidosis, shock, respiratory distress syndrome and hypomagnesaemia.7 Prognostic factors that may predict poor outcomes in AlP poisoning cases include hyperglycaemia, hypo- tension, acidosis, leukocytosis, hyperuricaemia, electro- cardiography abnormalities, high Acute Physiology and Chronic Health Evaluation scores, high Simplified Acute Physiology Scores, low Glasgow coma scale scores, acute renal failure, low prothrombin rates, methaemoglobin- aemia and the use of inotropes and mechanical vent- ilation.10–14 Serial blood glucose monitoring is a conv- enient and easy method of assessing hypo- or hyper- glycaemia, particularly in primary healthcare settings with limited resources. The current study aimed to determine the incidence of blood glucose level alter- ations in patients with AlP poisoning and the correl- ations between blood glucose levels and alterations and mortality. Methods This prospective observational study was conducted at the Postgraduate Institute of Medical Education & Research, a tertiary referral centre in Chandigarh, northeast India, from January 2010 to June 2011. All patients presenting to the emergency department during this period with a definitive history of AlP ingestion or symptoms comp- atible with AlP poisoning—including vomitus smelling of decaying fish or garlic, severe hypotension or shock, metabolic acidosis and abnormalities in cardiac rate or rhythm—were included in the study. Cases in which the ingestion of AlP was doubtful or with concom- itant ingestion of other drugs or alcohol were excluded, as were patients with a history of dextrose administration prior to presentation or those with diabetes mellitus. The vital signs of the patients were assessed, including their blood pressure (BP), heart rate and respiratory rate. Temperature and oxygen saturation were recorded using a pulse oximeter. Blood glucose levels were recorded using the Hitachi Modular Analytics System P800 chem- istry analyser (Roche Diagnostics K.K., Tokyo, Japan), after appropriate calibration and quality control measures. Alterations in blood glucose levels were defined as the occurrence of either hyperglycaemia (random blood gluc- ose levels of >200 mg/dL) or hypoglycaemia (random blood glucose levels of <55 mg/dL) at admission or any point during hospital stay.15,16 A complete blood count was performed along with biochemical tests to determine serum sodium, potassium, urea, creatinine and bilirubin levels. Arterial blood gas (ABG) analyses were performed to determine pH, partial pressure of oxygen, bicarbonate value, partial pressure of carbon dioxide and base excess for the given fraction of inspired oxygen. All clinical and laboratory measurements were recorded at admission, every six hours thereafter for the first 72 hours and then every 24 hours until discharge. If necessary, certain variables were assessed more frequently, depending on the clinical condition of the patient. All patients received standard supportive treatment, including basic emergency medical care and gastro- intestinal decontamination (i.e. gastric lavage). Hypo- glycaemic patients were treated with rapid intravenous infusions of two units of 100 mL of 25% dextrose solution and then maintained with 5% dextrose or 5% dextrose and normal saline solution, titrated according to electrolyte levels and glycaemic status.17,18 A maximum of two units of 5% dextrose and normal saline solution up to a total of 500 mL daily were admin- istered as a maintenance regimen for euglycaemic patients, titratred according to the patient’s input-output status. Hyperglycaemic patients were treated initially according Arvind Sharma, Prasanth Balasubramanian, Kiran D. Gill and Ashish Bhalla Clinical and Basic Research | e301 to a continuous insulin infusion protocol and, subseq- uently, via a subcutaneous insulin regimen.19 The statistical analysis was performed using the Statistical Package for the Social Sciences (SPSS), Version 22.0 (IBM Corp., Armonk, New York, USA). Various clinical and laboratory parameters were compared bet- ween survivors and non-survivors, with the primary vari- ables of interest being blood glucose level at presentation and the frequency of blood glucose alterations at adm- ission or during hospital stay. The normality of quant- itative variables was determined using the Kolmogorov- Smirnov test. For normally distributed data, means and standard deviations were calculated for continuous variables while frequencies, percentages and proportions were calculated for qualitative variables. A t-test was used to compare the mean differences between the study groups and a Chi-squared test was used to compare proportions. Univariate and multivariate logistic regression analyses were conducted with mortality as the dependent variable. Independent variables found to be significant on the univariate analysis were included in the logistic regression model and analysed using the Enter method. Random blood glucose levels were considered to be a continuous variable in the univariate and multivariate regression analyses, whereas alterations in blood gluc- ose levels were considered categorical (i.e. nominal) variables. A P value of <0.050 was considered statist- ically significant. This study was conducted with prior approval from the institutional ethics committee. Written informed consent was obtained from all patients or their relatives prior to participation in the study. Results A total of 116 cases of AlP poisoning were identified. Of these, 59 patients (51%) were 15–25 years old, 32 (28%) were 26–35 years old, 14 (12%) were 36–45 years old, nine (8%) were 46–55 years old and two (2%) were over 55 years old. The most frequent symptoms were vomiting (99%) and epigastric pain (61%), followed by dyspnoea (41%) and altered sensorium (28%). The median length of hospital stay was 18 hours (range: 5–42 hours). At presentation, 12 (10%) patients had hypoglycaemia, 16 (14%) had hyperglycaemia and 88 (76%) had normal blood glucose levels. In total, 57 patients (49%) survived and 59 patients (51%) died. The cause of death was refractory cardiogenic shock in 20 patients (34%), multiorgan dysfunction syndr- ome in six patients (10%), cardiac arrhythmias in five patients (8%) and respiratory failure in four patients (7%). The cause of death in the remaining 24 cases (41%) could not be determined. In terms of blood glucose alterations, all of the patients with hyperglycaemia, nine patients (75%) Table 1: Characteristics of patients with aluminium phosphide poisoning (N = 116) Variable Mean ± SD P value Survivors (n = 57) Non- survivors (n = 59) Sociodemographic characteristic Age in years 28 ± 9 30 ± 11 0.399 Male gender, n (%) 38 (67) 33 (56) 0.235 Form of AlP ingested, n (%) Powder 40 (70) 51 (86) 0.051Tablet 11 (19) 3 (5) Unknown 6 (11) 5 (9) Vital signs at admission Heart rate in bpm 101 ± 14 109 ± 11 0.001 SBP in mmHg 106 ± 29 77 ± 20 <0.001 Glasgow coma score 12.9 ± 0.1 2.3 ± 0.8 <0.001 Blood glucose measurements Blood glucose level* in mg/dL 119.9 ± 35.7 159.7 ± 92.5 <0.001 Frequency of blood glucose alterations,† n (%) 3 (5) 25 (42) <0.001‡ Biochemistry results Serum sodium in mmol/L 142.5 ± 7.0 144.6 ± 7.4 0.058 Serum potassium in mmol/L 4.0 ± 0.7 4.1 ± 1.1 0.216 Serum creatinine in mg/dL 0.8 ± 1.0 1.4 ± 1.2 0.003 Serum bilirubin in mg/dL 0.9 ± 0.6 0.8 ± 0.5 0.116 TLC × 103 per mm3 8.6 ± 3.4 12.2 ± 5.1 0.005 ABG measurements pH 7.3 ± 0.7 7.1 ± 1.3 <0.001 HCO3 16.3 ± 4.8 11.3 ± 5.6 <0.001 Presentation/hospital stay characteristics Median interval between ingestion and presentation in hours (IQR) 4 (3–6) 4 (2–7) 0.816§ Median dextrose administered in g (IQR) 62 (25–125) 75 (43–106) 0.856§ Median LOS in hours (IQR) 36 (24–66) 5 (2–12) <0.001§ SD = standard deviation; AlP = aluminium phosphide; bpm = beats per minute; SBP = systolic blood pressure; TLC = total leukocyte count; ABG = arterial blood gas; HCO 3 = bicarbonate; IQR = interquartile range; LOS = length of stay. *Assessed via random blood glucose tests. †Defined as either hyper- glycaemia (random blood glucose levels of >200 mg/dL) or hypo- glycaemia (random blood glucose levels of <55 mg/dL). ‡Using a Mann-Whitney U test. §Using a Chi-squared test. Prognostic Significance of Blood Glucose Levels and Alterations Among Patients with Aluminium Phosphide Poisoning e302 | SQU Medical Journal, August 2018, Volume 18, Issue 3 with hypoglycaemia and 34 patients (39%) with normal blood glucose levels died. Both mean blood glucose levels (159.7 ± 92.5 mg/dL versus 119.9 ± 35.7 mg/dL; P <0.001) and the frequency of blood glucose alterations (5% versus 42%; P <0.001) were significantly higher among non-survivors comp- ared to survivors. This was also the case for heart rate (109 ± 11 beats per minute [bpm] versus 101 ± 14 bpm; P = 0.001), total leucocyte count (12.2 ± 5.1 × 103 per mm3 versus 8.6 ± 3.4 × 103 per mm3; P = 0.005) and serum creatinine levels (1.4 ± 1.2 mg/dL versus 0.8 ± 1.0 mg/dL; P = 0.003). In addition, non-survivors had significantly lower systolic BP at admission (77 ± 20 mmHg versus 106 ± 29 mmHg), Glasgow coma scale scores (2.3 ± 0.8 versus 12.9 ± 0.1), arterial blood gas pH (7.1 ± 1.3 versus 7.3 ± 0.7) and bicarbonate values (11.3 ± 5.6 versus 16.3 ± 4.8) and median duration of hospital stay (5 versus 36 hours) compared to survivors (P <0.001 each) [Table 1]. Statistically significant variables from the univariate analysis were subsequently included in a logistic regr- ession model to predict mortality at a 95% confidence interval. Although systolic BP at admission (P = 0.029) and duration of hospital stay (P = 0.008) remained significant, neither blood glucose levels nor blood glucose alterations were found to be independent predictors of mortality (P >0.050 each) [Table 2]. Discussion According to international recommendations, blood glucose levels should be maintained at 140–180 mg/dL for normoglycaemic patients and 180–200 mg/dL for previously diabetic individuals.20 Both the hypo- and hyperglycaemic effects of AlP are attributable to the wide variety of changes in magnesium, calcium, phosphate, citrate and cortisol levels that result from AlP poisoning.11,21 These biochemical changes can act as either stimulatory or inhibitory modulators of the enzymes and hormones that catalyse and regulate the metabolism of glucose. Therefore, depending on the type of biochemical change, AlP poisoning can result in the elevation or decrease of blood glucose levels or neither.11,21 Nevertheless, the specific mechanism by which AlP poisoning causes hypoglycaemia is poorly under- stood. Possible explanations include as a result of liver damage due to the release of PH3 gas and the toxic effects of PH3 on the adrenal cortex, leading to decreased cor- tisol levels.22 In addition, certain symptoms of AlP pois- oning such as recurrent vomiting and lack of appetite may also play a role in the development of hypogly- caemia. In contrast, hyperglycaemia occurs due to either the stimulation of cortisol, glucagon and adrenaline secr- etion or the inhibition of insulin synthesis.11,21 A glucose- insulin-potassium infusion has been suggested as a pot- ential therapeutic modality in the treatment of hyper- glycaemia in AlP poisoning.23 Among critically-ill patients, blood glucose alter- ations have been associated with prolonged hospital stays as well as increased mortality.20,24 However, to the best of the authors’ knowledge, only one previous study has examined the relationship between hyperglycaemia and AlP poisoning outcomes. Mehrpour et al. published a prospective study of 45 patients with acute AlP pois- oning, of which 32 patients (71%) died.11 Non-survivors had significantly higher mean blood glucose levels than survivors (222.6 ± 20 mg/dL versus 143.4 ± 13.7 mg/dL; P = 0.021). Furthermore, blood glucose levels were an independent predictor of mortality in a multivariate analysis.11 This contradicts the findings of the current study in which alterations in blood glucose levels (i.e. either hyperglycaemia or hypoglycaemia) were not independent predictors of mortality. This may be because Mehrpour et al. utilised a different cut- off value to indicate hyperglycaemia than that of the present study (>140 mg/dL versus >200 mg/dL).11 Table 2: Logistic regression model to predict mortality among patients with aluminium phosphide poisoning (N = 116) Predictor Regression coefficient SE OR (95% CI) P value Heart rate −0.009 0.050 0.991 (0.899–1.093) 0.860 SBP −0.080 0.037 0.923 (0.859–0.992) 0.029 Glasgow coma score −0.586 0.454 0.557 (0.229–1.355) 0.197 Blood glucose level* 0.012 0.009 1.012 (0.994–1.031) 0.187 Blood glucose alterations† 2.036 1.544 7.662 (0.372–157.919) 0.187 Serum creatinine level 0.293 0.594 1.340 (0.418–4.294) 0.623 TLC 0.000 0.000 1.000 (1.000–1.000) 0.913 ABG pH −1.760 3.620 0.172 (0.000–207.369) 0.627 ABG HCO3 −0.045 0.135 0.956 (0.734–1.246) 0.741 Duration of LOS −0.094 0.035 0.910 (0.850–0.976) 0.008 SE = standard error; OR = odds ratio; CI = confidence interval; SBP = sys- tolic blood pressure; TLC = total leukocyte count; ABG = arterial blood gas; HCO 3 = bicarbonate; LOS = length of stay. *Assessed via random blood glucose tests. †Defined as either hyperglycaemia (random blood glucose levels of >200 mg/dL) or hypoglycaemia (random blood glucose levels of <55 mg/dL). Arvind Sharma, Prasanth Balasubramanian, Kiran D. Gill and Ashish Bhalla Clinical and Basic Research | e303 Strengths of the current study include its sample size and the evaluation of both hyper- and hypogly- caemia as predictors of mortality. However, the results are limited by the absence of any long-term follow-up of the survivors and the lack of analysis of other factors which may play a role in glucose homeostasis, such as serum calcium, magnesium, phosphate, insulin and cor- tisol levels. Conclusion As a result of several complex mechanisms, AlP poisoning can cause both hyper- and hypoglycaemia. However, the role of blood glucose levels and blood glucose alter- ations in predicting patient outcomes in AlP poisoning cases remains inconclusive. The authors recommend that further studies with larger sample sizes be conducted to evaluate other factors involved in glucose homeostasis. c o n f l i c t o f i n t e r e s t The authors declare no conflicts of interest. f u n d i n g No funding was received for this study. References 1. Murali R, Bhalla A, Singh D, Singh S. Acute pesticide poisoning: 15 years experience of a large north-west Indian hospital. Clin Toxicol (Phila) 2009; 47:35–8. doi: 10.1080/15563650701885807. 2. Banjaj R, Wasir HS. Epidemic aluminium phosphide poisoning in Northern India. Lancet 1988; 1:820–1. doi: 10.1016/S0140-6736 (88)91676-5. 3. Price NR, Mills KA, Humphries LA. Phosphine toxicity and catalase activity in susceptible and resistant strains of lesser grain borer (Rhyzopertha dominica). Comp Biochem Physiol C Phar- macol Toxicol Endocrinol 1982; 73:411–13. doi: 10.1016/0306- 4492(82)90144-7. 4. Bolter CJ, Chefurka W. Extramitochondrial release of hydrogen peroxide from insect and mouse liver mitochondria using the respiratory inhibitors phosphine, myxothiazol, and antimycin and spectral analysis of inhibited cytochromes. Arch Biochem Biophys 1990; 278:65–72. doi: 10.1016/0003-9861(90)90232-N. 5. Burgess JL, Morrissey B, Keifer MC, Robertson WO. Fumigant- related illnesses: Washington State’s five-year experience. J Toxi- col Clin Toxicol 2000; 38:7–14. doi: 10.1081/CLT-100100909. 6. Curry AS, Price DE, Tryhorn FG. Absorption of zinc phosphide particles. Nature 1960; 184:642–3. doi: 10.1038/184642a0. 7. Mehrpour O, Jafarzadeh M, Abdollahi M. A systematic review of aluminium phosphide poisoning. Arh Hig Rada Toksikol 2012; 63:61–73. doi: 10.2478/10004-1254-63-2012-2182. 8. Chugh SN, Ram S, Chugh K, Malhotra KC. Spot diagnosis of aluminium phosphide ingestion: An application of a simple test. J Assoc Physicians India 1989; 37:219–20. 9. European Food Safety Authority. Conclusion on the peer review of the pesticide risk assessment of the active substance calcium carbide. Eur Food Saf Author J 2011; 9:2419. doi: 10.2903/j. efsa.2011.2419. 10. Bogle RG, Theron P, Brooks P, Dargan PI, Redhead J. Aluminium phosphide poisoning. Emerg Med J 2006; 23:e3. doi: 10.1136/ emj.2004.015941. 11. Mehrpour O, Alfred S, Shadnia S, Keyler DE, Soltaninejad K, Chalaki N, et al. Hyperglycemia in acute aluminum phosphide poisoning as a potential prognostic factor. Hum Exp Toxicol 2008; 27:591–5. doi: 10.1177/0960327108096382. 12. Mostafazadeh B, Pajoumand A, Farzaneh E, Aghabiklooei A, Rasouli MR. Blood levels of methemoglobin in patients with aluminum phosphide poisoning and its correlation with patient’s outcome. J Med Toxicol 2011; 7:40–3. doi: 10.1007/s13181-010- 0121-7. 13. Shadnia S, Mehrpour O, Soltaninejad K. A simplified acute phys- iology score in the prediction of acute aluminum phosphide poisoning outcome. Indian J Med Sci 2010; 64:532–9. 14. Louriz M, Dendane T, Abidi K, Madani N, Abouqal R, Zeggwagh AA. Prognostic factors of acute aluminum phosphide poisoning. Indian J Med Sci 2009; 63:227–34. doi: 10.4103/0019-5359.53386. 15. Qaseem A, Humphrey LL, Chou R, Snow V, Shekelle P. Use of intensive insulin therapy for the management of glycemic control in hospitalized patients: A clinical practice guideline from the American College of Physicians. Ann Intern Med 2011; 154:260–7. doi: 10.7326/0003-4819-154-4-201102150-00007. 16. Klonoff DC, Alexander Fleming G, Muchmore DB, Frier BM. Hypoglycemia evaluation and reporting in diabetes: Importance for the development of new therapies. Diabetes Metab Res Rev 2017; 33:e2883. doi: 10.1002/dmrr.2883. 17. Alsahli M, Gerich JE. Hypoglycemia. Endocrinol Metab Clin North Am 2013; 42:657–76. doi: 10.1016/j.ecl.2013.07.002. 18. Cryer PE, Axelrod L, Grossman AB, Heller SR, Montori VM, Seaquist ER, et al. Evaluation and management of adult hypo- glycemic disorders: An Endocrine Society clinical practice guide- line. J Clin Endocrinol Metab 2009; 94:709–28. doi: 10.1210/jc. 2008-1410. 19. McDonnell ME, Umpierrez GE. Insulin therapy for the manage- ment of hyperglycemia in hospitalized patients. Endocrinol Metab Clin North Am 2012; 41:175–201. doi: 10.1016/j.ecl. 2012.01.001. 20. Aramendi I, Burghi G, Manzanares W. Dysglycemia in the critically ill patient: Current evidence and future perspectives. Rev Bras Ter Intensiva 2017; 29:364–72. doi: 10.5935/0103- 507X.20170054. 21. Abder-Rahman H. Effect of aluminum phosphide on blood glucose level. Vet Hum Toxicol 1999; 41:31–2. 22. Chugh SN, Ram S, Sharma A, Arora BB, Saini AS, Malhotra KC. Adrenocortical involvement in aluminium phosphide poisoning. Indian J Med Res 1989; 90:289–94. 23. Hassanian-Moghaddam H, Zamani N. Therapeutic role of hyper- insulinemia/euglycemia in aluminum phosphide poisoning. Medicine (Baltimore) 2016; 95:e4349. doi: 10.1097/MD.000000 0000004349. 24. Fahy BG, Sheehy AM, Coursin DB. Glucose control in the intensive care unit. Crit Care Med 2009; 37:1769–76. doi: 10.10 97/CCM.0b013e3181a19ceb. https://doi.org/10.1080/15563650701885807 https://doi.org/10.1016/S0140-6736%2888%2991676-5 https://doi.org/10.1016/S0140-6736%2888%2991676-5 https://doi.org/10.1016/0306-4492%2882%2990144-7 https://doi.org/10.1016/0306-4492%2882%2990144-7 https://doi.org/10.1016/0003-9861%2890%2990232-N https://doi.org/10.1081/CLT-100100909 https://doi.org/10.1038/184642a0 https://doi.org/10.2478/10004-1254-63-2012-2182 https://doi.org/10.2903/j.efsa.2011.2419 https://doi.org/10.2903/j.efsa.2011.2419 https://doi.org/10.1136/emj.2004.015941 https://doi.org/10.1136/emj.2004.015941 https://doi.org/10.1177/0960327108096382 https://doi.org/10.1007/s13181-010-0121-7 https://doi.org/10.1007/s13181-010-0121-7 https://doi.org/10.4103/0019-5359.53386 https://doi.org/10.7326/0003-4819-154-4-201102150-00007 https://doi.org/10.1002/dmrr.2883 https://doi.org/10.1016/j.ecl.2013.07.002 https://doi.org/10.1210/jc.2008-1410 https://doi.org/10.1210/jc.2008-1410 https://doi.org/10.1016/j.ecl.2012.01.001 https://doi.org/10.1016/j.ecl.2012.01.001 https://doi.org/10.5935/0103-507X.20170054 https://doi.org/10.5935/0103-507X.20170054 https://doi.org/10.1097/MD.0000000000004349 https://doi.org/10.1097/MD.0000000000004349 https://doi.org/10.1097/CCM.0b013e3181a19ceb https://doi.org/10.1097/CCM.0b013e3181a19ceb