ORGANOPOSPHATE POISONING

ORGANOPHOSPHATE AND CARBAMATE INSECTICIDE SPOSONING

Organophosphate and carbamate insecticides are widely used in agriculture (For crop spray) and at home as insecticides for rodents, cockroach etc. Parathion, DDT, Finis, Baygon, Coopex are commonly used products. Most of the war gases are also organophosphates.

Mode of Action

 Organophosphates and carbamates are also called anticholinestrases because they inhibit the enzyme anticholinestrase resulting in an increased acetylcholine activity at nicotinic and muscarinic receptors and in the central nervous system.

Intoxication may follow:

·         Ingestion (for suicide or accidentally).

·         Inhalation (usually when spraying crops or even at home using insecticide spray for cockroaches and other insects)

·         Dermal absorption

CLINICAL FEATURES

Time from exposure to the onset of toxicity varies from minutes to hours but usually is between 30 min to 2 hours. Most patients recover within 24-48 hours but some insecticides may affect for weeks to months.

Muscarinic effects:

·         GIT:    nausea, vomiting, abdominal  colic, diarrhea, tenesmus (due to increased gut motility) sweating, hypersalivation and fecal incontinence.

·          

RESP: dyspnea, cough, wheezing, increased bronchial secretions, pulmonary edema. Death is usually due to respiratory arrest.

·         Urinary: increased urinary frequency and incontinence.

·         EYE:    Miosis, blurred vision.

·         Heart:   bradycardia, hypotension, heart block in severe cases.

Nicotinic effects:

·         Muscle twitching, fasciculations and muscle weakness. In severe cases paralysis of limb, respiratory and extraocular muscles.

·         Hypertension and tachycardia.

CNS effects:

Anxiety, restlessness, tremor, convulsions, confusion and coma.

COMPLICATIONS:

1.       Loss of consciousness

2.       Respiratory failure (due to aspiration, excessive secretions, pneumonia, septicemia or ARDS). Cause of death is usually respiratory failure.

3.       Aspiration pneumonia: due to vomiting in altered consciousness may be aspirated.

4.       Urinary tract infection.

5.       Septicemia.

DIAGNOSIS

Usually the diagnosis is clinical. History is available from the patient or relatives. It may be confirmed by measuring RBC and plasma cholinesterase activity: a reduction of cholinesterase activity in red blood cells and plasma to less than 50% of normal confirms the diagnosis of organophosphate poisoning.

MANAGEMENT

Oxygen: Admit the patient in ICU and give supplementary oxygen.

Gastric lavage: If the agent was recently ingested, empty the stomach by gastric lavage and administer activated charcoal.

·         Do not induce vomiting because of risk abrupt onset of seizures and aspiration.

·         If the insecticide is one the victim’s skin or hair, wash with soap and water.

Atropine:  Atropine reverses excessive muscarinic stimulation and is effective treatment of salivation wheezing, abdominal cramp and sweating.

Administer atropine 2 mg IV every 15 min until bronchial and other secretions are controlled. Repeated doses or constant atropine infusion (0.02-0.08 mg/kg/hour) may be necessary for several days. Atropine causes tachycardia, if heart rate is more than 130/min then for protection of heart reduce the heart rate with IV diltiazem or propranolol (we have IV verapamil instead of diltiazem and metroprolol instead of propranolol in Pakistan).

Pralidoxime (Contrathion):  It is a specific antidote that reactivates cholinestrases and is indicated for nicotinic symptoms due to organophosphate poisoning.

Dose is 1-2 g IV over 5-20 min (one vial of Contrathion contains 200 mg Pralidoxime and costs Rs. 500)   i-e. 5-10 vials of Contrathion are diluted in 100 ml of water for injection. The dose may be repeated every 4-6 hours or start continuous infusion at the rate of 10 mg/kg/hr. Continue Pralidoxime as long as there is any evidence of acetylcholine excess.

(Signs of full atropinization: dry hot skin, dry secretions, pulse more then 70/min and dilated pupils).

Mechanical ventilation:

Indication

·         Excessive secretions

·         Depressed level of consciousness: to protect the airway.

·         Poor gas exchange unresponsive to supplementary oxygen.

·         Severe metabolic acidosis with hemodynamic instability (systolic BP<90 mmHg).

Mode of ventilator

SIMV + pressure support mode in either pressure controlled or volume controlled form. Positive end expiratory pressure is applied to keep oxygen saturation >94% at FIO2 40%.

Weaning from ventilator is usually carried out with pressure support weaning and T-tube trial.

Types of Heart Failuer

The Heart Failure may be classified in several ways.

1.       Acute versus chronic heart failure

2.       Left versus right and biventricular failure

3.       Forward versus backward failure

4.       Systolic versus diastolic failure

5.       Low output versus high output failure

Acute versus chronic heart failure:

Acute heart failure:

Heart failure developing suddenly in hours or days in a previously asymptomatic patient is called acute heart failure.

Chronic heart failure:

Heart failure developing gradually is called chronic heart failure. In this type of failure a variety of compensatory changes may take place in early phase to improve cardiac function. These adaptive mechanisms allow the patient to adjust and tolerate not only the anatomic abnormality but also a reduction in cardiac output with less difficulty.

Left versus right & biventricular heart:

Left sided heart failure:

Left-sided heart failure is characterized by reduction in effective left ventricular output for a given pulmonary venous or left atrial pressure.

An acute increase in left atrial pressure may cause pulmonary congestion or pulmonary edema, while chronic increase in left atrial pressure leads to reflex pulmonary vasoconstriction which protects increasing pulmonary hypertension (as a compensatory mechanism).

Causes of left heart failure

·         Ischemic heart disease (commonest)

·         Systemic hypertension

·         Mitral and aortic valve disease

·         Cardiomyopathies

Right sided heart failure:

Right-sided heart failure is characterized by reduction in right ventricular output for any given right atrial pressure. The increased right atrial pressure is manifested as an increased jugular venous pressure and as hepatic congestion.

Causes of right heart failure:

·         Secondary to left heart failure (most common)

·         Chronic lung disease (causing cor-pulmonale)

·         Pulmonary embolism or pulmonary hypertension

·         Tricuspid and pulmonary valve disease

·         ASD & VSD

·         Right ventricular cardiomyopathy

Biventricular or congestive cardiac failure (CCF)

When both sides of heart are involved, features of both right and left heart failure are present. In most of the patient right heart failure is a result of preexisting left heart failure.

Forward versus backward failure:

Forward failure:

In some patients with cardiac failure predominant problem in an inadequate cardiac output that leads to diminished perfusion of vital organs leading to ischemia of theses organs is called forward failure. Ischemia of brain causes mental confusion, ischemia of skeletal muscles leads to weakness, ischemia of kidneys causes sodium and water retention leading to symptoms of heart failure.

Backward failure:

In some patients cardiac failure presents mainly with features of damming of blood into venous system such as lung congestion in left heart failure and congestion of liver, spleen and other areas in right heart failure.

Systolic versus diastolic failure:

In majority of patients heart failure is due to combined systolic and diastolic dysfunction, however isolated systolic or diastolic dysfunction may be present.

Systolic failure:

Heart failure may develop as a result of impaired myocardial contraction (systolic dysfunction). The most common cause of systolic ventricular dysfunction is ischemic heart disease usually after myocardial infarction. The left ventricle is usually dilated and fails to contract normally resulting in symptoms of predominantly forward failure.

Diastolic failure:

Heart failure may develop due to poor ventricular filling caused by impaired ventricular relaxation (diastolic dysfunction). The most common cause is left ventricular hypertrophy as a result of hypertension and coronary artery disease. Other causes of diastolic dysfunction are hypertrophic and restrictive cardiomyopathy, diabetes and pericardial disease.

Diastolic failure is common in elderly, women and in patients with history of hypertension. It is a common cause of patient’s visit to doctor, patients present with shortness of breath and there is history of hypertension only (usually no history of previous MI).

Low versus high cardiac output failure:                                                                                          

Low output failure:

Low cardiac output at rest or during exertion characterizes heart failure caused by common conditions such as congenital, valvular, rheumatic, hypertensive, coronary and cardiomyopathic diseases. Low output failure presents with evidence of systemic vasoconstriction such as cold, paler or cyanotic extremities. Pulse pressure is low.   

High cardiac output failure:

Conditions that are associated with a very high cardiac output such as anemia, beriberi, paget’s disease of bone and thyrotoxicosis may lead to or precipitate heart failure.

The extremities are usually warm, and flushed and pulse pressure is wide or normal. Detail of high output failure are given at the end of this section.

Chronic Heart Failure:

Heart failure developing is called chronic heart failure. In this type of failure a variety of compensatory changes may take place in early phases to improve cardiac function. These adaptive mechanisms allow the patient to adjust to and tolerate not only the anatomic abnormality but also a reduction in cardiac output with less difficulty.

As the disease progresses these compensatory mechanisms fail to improve cardiac function.

 In compensated cardiac failure, patient has impaired cardiac function but the adaptive or compensatory changes prevent the development of overt cardiac failure. Theses compensatory changes are increased heart rate, hypertrophy of cardiac muscles an dilatation of heart chambers. Acute cardiac failure is uncompensated and therefore more symptomatic because time is required to develop theses compensatory changes to develop.

COMPENSATORY OR ADAPTIVE MECHANISMS IN THE HEART FAILURE:

A number of compensatory changes occur in the cardiovascular system in chronic heart failure to maintain adequate blood flow to the vital organs of the body as following:

MECHANISM                               ADVANTAGE                                        DISADVANTAGE              

                                                                                                                                      IN LONG TERM

Sympathetic stimulation               increased heart rate (as cardiac output                  Increases energy expenditure  

                                                                Depends on stroke volume and heart rate).

                                                                Sympathetic stimulation causing increased         

                                                                Arterial tone, increased heart rate and

                                                                Increased ventricular contractility.

Remodeling                                        Ventricular hypertrophy and dilatation to             Leads to deterioration and death

                                                      Maintain adequate blood flow.                                               Of cardiac cells

Fluid water retention due            Increases ventricular filling pressure                       Cause pulmonary congestion

To stimulation of rennin-              (augment preload)                                                         

angiotensin system

The clinical features in cardiac failure are based on the two factors:

Reduced cardiac output (forward failure)

This results from decreased heart function. This reduced output leads to diminished filling of arterial tree, resulting in ischemia of the organs.

Damming of blood (backward failure)

Heart becomes fail o pump the whole blood coming to it, resulting in damming of blood back into venous system, organs become congested & their functions are distributed.

In majority of patients there is combination of both factors mentioned above.

http://doctor-tips-for-health.blogspot.com/2011/06/chronic-liver-disease-cld.html

CHEST PAIN DUE TO MUSCULOSKELETAL DISORDERS:

CHEST PAIN DUE TO MUSCULOSKELETAL DISORDERS:

Localized tenderness is common. Pain may be sharp, lasting for few seconds or it may be dull that persists for hours or even days. Pain is variable in site and intensity; there is no definite pattern. It may vary with posture or movement, but does not cease instantly on rest. Pain due to cervical spondylosis is very common.

Local tenderness over rib or costal cartilage is usually present.

CHEST PAIN DUE TO AORTIC DESSECTION:

Hypertension and Marfan’s syndrome are the most common predisposing factors. Patient is usually old presenting with severe tearing chest pain radiating to interscapular region, not responding to anti-anginal treatment. Pulse may be unequal. Features of cardiac temponad or acute aortic regurgitation may be present. Chest x-ray may show wide mediastinum. Transesophageal echocardiogram (TEE), CT or MRI are helpful in diagnosis.

CHEST PAIN DUE TO EMOTIONAL CAUSES:

Emotional disorders may cause chest discomfort in the form of chest tightness, lasting for half and hour or more that in unrelated to exertion. It may be sharp and very vrief and located near the left nipple. This type of pain is also called “precordial catch” effort syndrome or Da Costa’s syndrome”. Emotional strain may be evident or not. This type of pain is common in females of our society. However never underestimate the young population because this chest pain may be a real problem as a result of mitral valve prolapse (MVP), aortic stenosis or hypertrophic cardiomyopathy.

Therefore always rule out all possibilities before declaring pain due to emotional disturbance, hysteria or malingering.

 

Written by

Dr. M. Inam Danish

PATIENT EVALUATION AND PLAN (Medical Students should be Check )

PATIENT EVALUATION AND PLAN

Always rule out life threatening conditions such as myocardial infarction, aortic dissection, pulmonary embolism and pneumothorax.

History is very important, ask about risk factors for MI such as hypertension, smoking, diabetes, dyslipidemia and strong family tendency. Decide whether the pain is typical or atypical. For pulmonary embolism ask about prolonged bed rest, DVt, use of oral contraceptives and valvular heart disease. History of heartburn and food regurgitation may indicate reflux esophagitis. Ask about any emotional problem. Sudden chest pain with shortness of breath, especially in patients of asthma, tuberculosis and COPD may indicate pneumothorax. While examining the patient auscultation of lung and heart may be helpful. Local tenderness indicates musculoskeletal disorder.

CHEST PAIN DUE TO PERICARDITIS:

• Visceral pericardium and most of the parietal pericardium is insensitive to pain, therefore pain associated with pericardium is believed to be due to inflammation of adjacent parietal pleura. Pain due to non-infectious causes such as MI or uremia is mild while infectious pericarditis causes more sever pain due to spread of infection to the neighboring pleura.
• Pain due to pericarditis may be felt at the tip of the shoulder, neck, anterior chest, upper abdomen or back.
• Pericardial pain is aggravated by cough and deep inspiration because of pleural irritation, change in posture and swallowing. It become sharper and more left-sided in supine position and milder when patient sits upright and leans forward.
• In some patients pericardial pain is steady retrosternal discomfort mimicking the pian of myocardial infarction.

CHEST PAIN DUE TO PULMONARY EMBOLISM:

Infarction of a lung that is adjacent to the pleura commonly irritates pleural surface and causes chest discomfort, it may resemble the pain of myocardial infarction.

CHEST PAIN DUE TO ESOPHAGEAL CAUSES:

Esophageal spasm due to reflux esophagitis causes squeezing pain that mimics pain of MI. it may have similar pattern of distribution. History of heartburn and food regurgitation are important clues. A number of children come to cardiac emergency with chest pain that is usually due to esophageal spasm as result of eating groundnut in the form of sweat supari, pan or gutca. We can only pray to God to save our children as the government is not interested to stop such health-killing business. 

                                                                                                    Dr. Inam  Danish