|Year : 2016 | Volume
| Issue : 1 | Page : 31-34
Role of coconut oil and soda bicarbonate in gastric lavage in the management of celphos poisoning
Konsam Jina Devi1, Kasomhung Soreingam2, Vipin Kumar Singh3
1 Department of Anaesthesiology and Intensive Care, Regional Institute of Medical Sciences, Lamphelpat, Manipur, India
2 Department of Anaesthesiology, Jawaharlal Nehru Institute of Medical Sciences, Porompat, Imphal, Manipur, India
3 Department of Anaesthesiology and Intensive Care, King George Medical College, Lucknow, Uttar Pradesh, India
|Date of Web Publication||25-Feb-2016|
Konsam Jina Devi
c/o - Dr. Konsam Gopal Singh, Uripok Sinam Leikai, Rims Road, Imphal West - 795 001, Manipur
Source of Support: None, Conflict of Interest: None
Context: Celphos poisoning is one of the most common and lethal poison with no antidote available till now. Aims: To evaluate the effectiveness of new treatment regimen and interventions to reduce the mortality from celphos poisoning. Settings and Design: A profile of 30 patients with alleged intake of celphos tablets who got admitted in intensive care unit (ICU) was studied. Materials and Methods: In all the 30 patients with alleged celphos poisoning, extensive gastric lavage was done with a mixture of coconut oil and sodium bicarbonate solution. Strict monitoring, both invasive and noninvasive was done and symptomatic/supportive treatment was carried out on a patient-to-patient basis. Statistical Analysis: At the end of the study, all the data were compiled systematically and statistical analysis was carried out using the nonparametric tests and value of P < 0.05 was considered significant. Results: Majority of the patients were young with a mean age of 20.14 ± 3.62 years and had good educational level. Most of the patients presented clinically with cardiovascular signs and symptoms (60%), followed by respiratory distress (13.33%) and little higher incidence of multiorgan symptomatology (16.67%). The mean stay of the patients in ICU was 5.62 ± 1.24 days and the survival rate was 40%. Conclusions: With the treatment regimen we have formulated, we were able to save 40% of our patients and recommend the use of this regimen by all the intensivists and physicians.
Keywords: Aluminum phosphide, celphos, coconut oil, magnesium sulfate, sodium bicarbonate
|How to cite this article:|
Devi KJ, Soreingam K, Singh VK. Role of coconut oil and soda bicarbonate in gastric lavage in the management of celphos poisoning. J Health Res Rev 2016;3:31-4
|How to cite this URL:|
Devi KJ, Soreingam K, Singh VK. Role of coconut oil and soda bicarbonate in gastric lavage in the management of celphos poisoning. J Health Res Rev [serial online] 2016 [cited 2020 Apr 4];3:31-4. Available from: http://www.jhrr.org/text.asp?2016/3/1/31/177495
| Introduction|| |
Aluminum phosphide (AlP), also known as celphos is one of the most dreaded poisons encountered in toxicology. The salt is available in tablet and pellet forms. AlP poisoning is common in all parts of the world but is found more commonly in developing countries such as India and is often implicated in accidental and suicidal poisonings in India.,, The fatal dose is approximately 0.5 g and acute poisoning with these compounds may be direct due to ingestion of the salts or indirect from accidental inhalation of phosphine generated during their approved use. The reason for pre-approval for celphos poisoning was that in such cases, mortality is 100% and no time should be lost in resuscitation. Previously, the laws and legislations were not that strict and it was easily available in the counter but in the last few years stricter norms have reduced its availability, even though they are still not enough to reduce the suicidal rate due to its consumption, which traumatizes so many families. It is a highly toxic compound that releases phosphine gas on contact with moist surfaces and patients can present clinically with gastrointestinal (GI) hemorrhage, arrhythmias, shock, renal and hepatic failure, central nervous system disturbances, and ultimately leading to death in almost 100% of cases.,, Most patients who survived had either taken a very small amount or the tablet had been exposed to air, thus rendering it nontoxic. Patients remain mentally clear till cerebral anoxia due to shock supervenes resulting in drowsiness, delirium, and coma. Several electrocardiogram (ECG) changes ranging the period when ventricles are depolarized (ST) segment elevation/depression, the time the electrical impulse takes to travel from the sinus node through the AV node (PR) and the rapid depolarization of the right and left ventricles (QRS) interval prolongation, complete heart block to ectopics and fibrillation have been observed. Reversible myocardial injury has also been reported.,, The breath of patients who have ingested AlP has a characteristic garlic-like odor. Conformation of diagnosis is based on the patient's history and a positive result (blackening) on tests of the patient's breath with paper moistened with fresh silver nitrate solution or by chemical analysis of blood or gastric acid for phosphine. Celphos poisoning has always been a big headache and menace for the intensivists throughout the world probably due to nonavailability of its antidote and 100% mortality, which does not encourage the physicians to try whole heartedly to salvage the patients.
With all these facts, we devised an intervention of a mixture of coconut oil and soda bicarbonate in gastric lavage to make a solution of 100 mL. The aim was to see the efficacy of this medication combination in reducing the mortality due to celphos poisoning.
| Materials and Methods|| |
Approval from the Ethical Committee is taken. Thirty patients got admitted in the intensive care unit (ICU) of our institute over the last 2–3 years period with a history of intake of celphos (AlP). Most of them had features of cardiogenic shock, hypotension, and arrhythmias, whereas a few got admitted with respiratory distress and rest of them had multitude of symptoms related to different organ systems. On admission to ICU, monitors were attached for Heart Rate (HR), Non-Invasive Blood Pressure (BP), ECG, Pulse Oximetry (SpO2), and Endtidal carbon dioxide (EtCO2), and Ryle's tube was inserted through nasal route. The patients who were grossly unstable hemodynamically or had respiratory distress were induced with injection ketamine 2 mg/kg body weight and injection vecuronium bromide 0.1 mg/kg body weight. Endotracheal intubation was done and patients were put on mechanical ventilation. Gastric lavage was initiated with aliquots of 50 mL of coconut oil and 50 mL of sodium bicarbonate solution and continued for the next half an hour, with simultaneous aspiration being done after every 3–5 min through Ryle's tube. Coconut oil was just heated to lukewarm temperature so as to make a miscible solution with sodium bicarbonate. The procedure of gastric lavage was usually done 10–15 times in the first hour. An intravenous access through internal jugular vein was established for central venous pressure monitoring as well as for guiding the fluid therapy in majority of patients who had presented with cardiovascular instability, respiratory distress, and renal failure. In a few patients who had severe cardiogenic shock, an arterial line was also secured through radial/dorsalis pedis artery for observing beat-to-beat variation of HR and BP. Symptomatic treatment was initiated on a patient-to-patient basis. Magnesium sulfate, dopamine, dobutamine, levosimendan, amiodarone infusions, and other appropriate intravenous drugs were given depending on the patient's clinical presentation and symptomatology, as well as arrhythmias and BP variations. Urine output was also monitored. Patients who required mechanical ventilation were kept sedated with injection midazolam and paralyzed with injection vecuronium. During this period, strict and vigil monitoring of all vital parameters was done and treatment regimens were titrated according to the clinical condition of the patients. Gastric lavage was again performed after 1 h of admission with the same for the next half an hour.
After admission in the ICU, all the baseline routine and specific investigations were carried out including regular arterial blood gas analysis (ABG). Soda bicarbonate was given empirically to all patients in a dose of 1 mEq/kg body weight and further adjusted for correction of metabolic acidosis as per ABG reports. At the end of the study period, all the data were arranged systematically and were subjected to statistical analysis using nonparametric tests. Value of P < 0.05 was taken as significant value.
| Results|| |
In the last 2–3 years, 30 got admitted with an alleged history of celphos intake.
The demographic profile of these patients is shown in [Table 1].
The age of 30 patients who got admitted in the ICU ranged from 16 to 50 years, with a mean and standard deviation of 20.14 ± 3.62 years. There was not much significant difference on the gender basis as 17 males and 13 females were admitted with celphos consumption. The incidence of poisoning was surprisingly high with a significant proportion in the more educated class and who were nonworking (P < 0.05). The incidence was more in the families of moderate income, especially among the unmarried young members, which was statistically significant on analysis. The incidence of poisoning was evenly distributed among the rural and urban population and was considered to be a nonsignificant factor (P > 0.05) [Table 2].
The maximum number of patients presented clinically with cardiovascular instability, either in the form of hypotension or arrhythmias (60%), which was clinically quite significant (P < 0.05). Also, 13.33% of the patients presented with respiratory distress alone, whereas 16.67% of the patients had combined symptoms related to respiratory, cardiovascular system, or central nervous system. Rest of the patients got admitted with altered sensorium [Table 3].
Out of the 30 patients, 25 required mechanical ventilation and 80% of the patients required inotropic support for maintaining stable hemodynamic parameters. The mean stay in ICU varied from 2 to 10 days, with a mean stay of 5.62 days with an SD of 1.24. Also, 40% of the patients were saved which is quite significant, but the rest (60%) succumbed to their poisonings [Table 4]. The mortality rate varied from 20% to 100% and the mortality increased with progressive involvement of the number of organs. As shown in [Table 4], the mortality reaches 100% if four or more organs are involved, which is statistically significant (P < 0.05).
| Discussion|| |
Celphos is formulated as a greenish gray tablet of 3 g, which in the presence of moisture or HCl, releases
The residue, Al(OH) 3 is nontoxic AlP, when ingested, liberates a lot of phosphine (PH3) gas in the stomach, which has a very pungent smell. Phosphine gas is rapidly absorbed from the gastric mucosa and, once it gains access to bloodstream, it reaches various tissues and at cellular level inhibits the mitochondrial respiratory chain and hence leads to cell necrosis and death. It has been suggested that phosphine leads to noncompetitive inhibition of the cytochrome oxidase of mitochondria, blocking the electron transfer chain and oxidative phosphorylation, producing an energy crisis in the cells., Recently, Chugh et al. found inhibition of catalase and induction of superoxide dismutase enzymes by phosphine in humans, leading to free radical formation, lipid peroxidation, and protein denaturation of cell membrane, ultimately leading to hypoxic cell damage. This has been suggested to inhibit myocardial cellular metabolism and necrosis of the cardiac tissue, resulting in the release of reactive oxygen intermediates. Refractory myocardial depression from AlP toxicity is not uncommon and carries a very high mortality., These cardiotoxic effects were quite marked in our patients, as 80% of the patients required inotropic support. Cardiotoxicity/toxic chemical myocarditis is manifested as depressed left ventricular ejection fraction, ECG changes varying from ST segment elevation/depression, PR prolongation, broad QRS complexes, and right or left bundle branch block, supraventricular ectopics, or fibrillation. Biochemical changes include rise in aspartate transaminase, creatine phosphokinase-muscle/brain, and lactate dehydrogenase. Histopathology shows myocytolysis, multiple areas of necrosis, and congestion. Hypomagnesemia has been known to cause arrhythmias in AlP poisoning and magnesium supplementation has been suggested as a therapeutic option. The findings of our study do correlate with all the above studies, as most of our patients presented with arrhythmias of varying nature and it proved fatal in majority of the patients who died in our ICU. Majority of our patients were young, unmarried with male gender predominance, and poisoning was quite prevalent in the educated community, both from the rural and urban population, in almost equal proportions. The incidence was equal among working and the nonworking population, highlighting the fact that the employment stress is not the only factor but rather it is the social and family factors, which drive these people to commit suicide. Toxicity that occurs after inhalation is characterized by chest tightness, cough, and shortness of breath. Children may be more vulnerable because of relatively increased minute ventilation per kilogram and failure to evacuate an area promptly, when exposed. Furthermore, phosphine gas is eliminated through the lungs; hence, due to high concentration in the respiratory alveoli, it is responsible for direct alveolar damage. Large number of our patients also presented with respiratory distress, either alone or in combination with other organ dysfunction. Acute respiratory distress syndrome (ARDS) and exudative pleural effusions can develop. Studies in the past have shown increased levels of inflammatory markers (cytokines and interleukins) in ARDS, which increase the capillary permeability. This combined effect of increase in capillary permeability due to global hypoxia and ARDS could be responsible for the exudative effusion seen predominantly in the pleural cavity and not in other serous cavities. GI symptoms are usually the first to occur after exposure. Symptoms may include nausea, vomiting, abdominal pain, and diarrhea. Death due to acute hepatocellular toxicity and fulminant hepatic failure has also been reported in acute poisoning. Blood and protein in the urine, and acute kidney failure due to shock can occur. Analysis of blood gases may reveal combined respiratory and metabolic acidosis. Also, there have been reports of significant hypomagnesemia and hypermagnesemia associated with massive focal myocardial damage., Our findings are quite consistent with these facts as the mortality increased with increasing number of organ system involvement. Chronic exposures to very low concentrations may result in anemia, bronchitis, GI disturbances, and visual, speech, and motor disturbances. Gastric lavage is important in the initial stage. The management principles aim to sustain life with appropriate resuscitation measures until phosphine is excreted from the body. If phosphides have been ingested, do not induce emesis. Gastric lavage with saline or sodium bicarbonate or potassium permanganate (1:1000) has also been recommended by earlier studies. The rationale behind the use of a mixture of soda bicarbonate and coconut oil in our patients is guided by the chemical reaction of AlP with moisture and HCl, liberating phosphine gas, which rapidly gets absorbed through gastric mucosa.
As the poison itself causes a lot of gastric mucosal damage, it exposes a lot of raw area for phosphine absorption. The mechanism by which coconut oil reduces the toxicity of phosphides is unknown but most probably it forms a protective layer around the gastric mucosa, thereby preventing the absorption of phosphine gas. Secondly, it helps in diluting the HCl and again inhibiting the breakdown of phosphide from the pellet. Soda bicarbonate mainly neutralizes the HCl and thus diminishing the catalytic reaction of phosphide with HCl, thereby inhibiting the release of phosphine.
The main principles of treatment are the following.
- Carry out methods to absorb phosphine through GI tract and neutralizing the HCl with soda bicarbonate and coconut oil, as explained earlier
- Reduce organ toxicity with appropriate interventions
- Enhance phosphine excretion, especially through lungs, by increasing the respiratory rate, which becomes easier when the patient is paralyzed, sedated, and put on mechanical ventilation. This results in decreasing the basal metabolic rate of body and decreased oxygen requirement, thus compensating the actions of inhibited cytochrome oxidase to certain extent
- Phosphine is excreted through urine also. Therefore, adequate hydration and renal perfusion by low-dose dopamine 4-6 μg/kg/min must be maintained. Diuretics are not useful in the presence of profound shock
- Dobutamine 2–10 μg/kg/min can be used to increase the cardiac contractility. Levosimendan has been used in some cases; however, it has been shown to increase mortality in some cases. Amiodarone can be used to counteract the ventricular arrhythmias
- Supportive measures have to be taken.
Certain specific measures can be adopted to reduce the fatal episodes of AlP. These include the following.
- Role of hyperbaric oxygen can be studied especially in the background of inhibition of mitochondrial respiratory chain
- The gastroscope can be used to remove the undissolved pellet
- Water should not be used as a lavage agent
- Some highly pungent and nauseating substance may be added to the pellets
- Strict laws and legislations can be made regarding the free sales of the chemical
- Availability of single tablet pack encased in hard plastic material with hard spikes will be helpful
- Social awareness regarding handling of the substance and its lethal consequences is required
- Alternatives to celphos, which are less toxic and fatal, should be manufactured to serve the same purpose
- Lab research should be undertaken extensively to find out its antidote.
| Conclusions|| |
Antidotes for various fatal poisons have been developed over the last three decades, but even now this poison is killing the mankind. Although few lives have been saved here and there, doubt still remains about the nature of poison consumed, the amount of poison consumed, the time interval between consumption and resuscitation, and so on. With the treatment regime we have formulated, we were able to save 40% of our patients who had been admitted with a definite history of celphos poisoning. Six of our patients consumed three or more than three tablets of the celphos poison, whereas eight of the patients were brought to the hospital almost more than 6 h of ingestion of the celphos pellet, which we believe led to the increase of mortality rate among our patients. We recommend the use of this regimen by all the intensivists and physicians so as to possibly save the lives of so many patients from this hopeless situation.
| References|| |
Siwach SB, Yadav DR, Arora B, Dalal S, Jagdish. Acute aluminium phosphide poisoning: An epidemiological, clinical, and histopathological study. J Assoc Physicians India 1988;36:594-6.
Koley TF. Aluminium phosphide poisoning. Indian J Clin Pract 1988;9:14-22.
Gupta S, Ahlawat SK. Aluminium phosphide poisoning – a review. J Toxicol Clin Toxicol 1995;33:19-24.
Chugh SN, Dushyant, Ram S, Arora B, Malhotra KC. Incidence and outcome of aluminium phosphide poisoning in a hospital study. Indian J Med Res 1991;94:232-5.
Singh UK, Chakraborty B, Prasad R. Aluminium phosphide poisoning: A growing concern in pediatric population. Indian Paediatr 1997;34:650-1.
Chugh SN, Arora V, Kaur S, Sood AK. Toxicity of exposed aluminium phosphide. J Assoc Physicians India 1993;41:569-70.
Chefurka W, Kashi KP, Bond EJ. The effect of phosphine on electron transport in mitochondria. Pest Biochem Physiol 1976;6:65-84.
Sudakin DL. Occupational exposure to aluminium phosphide and phosphine gas: A suspected case report and review of the literature. Hum Exp Toxicol 2005;24:27-33.
Lall SB, Sinha K, Mittra S, Seth SD. An experimental study on cardiotoxicity of aluminium phosphide. Indian J Exp Biol 1997;35:1060-4.
Bogle RG, Theron P, Brooks P, Dargan PI, Redhead J. Aluminium phosphide poisoning. Emerg Med J 2006;23:e3.
Mathur A, Swaroop A, Aggarwal A. ECG changes in aluminium phosphide and organo phosphorus poisoning. Indian Pract 1999;52:249-52.
Karanth S, Nayyar V. Rodenticide-induced hepatotoxicity. J Assoc Physicians India 2003;51:316-7.
Suman RL, Savani M. Pleural effusion - a rare complication of aluminium phosphide poisoning. Indian Paediatr 1999;36:1161-3.
Chugh SN. Aluminium phosphide. In: Lall SB, editor. Essentials of Clinical Toxicology. New Delhi: Narosa Publishing House; 1998. p. 41-6.
Shadnia S, Rahimi M, Pajoumand A, Rasouli MH, Abdollahi M. Successful treatment of acute aluminium phosphide poisoning: Possible benefit of coconut oil. Hum Exp Toxicol 2005;24:215-8.
[Table 1], [Table 2], [Table 3], [Table 4]