INTEGRAL UNIVERSITY , LUCKNOW

Session:2019-2020

Assignment on: supportive care in clinical toxicology

Submitted by:. Submitted to:.

KAUSAL VERMA. MR.Mohd.AJMAL

PHARM.D. Assistant professor

1601096009. Faculty of pharmacy

 SUPPORTIVE CARE IN CLINICAL TOXICOLOGY

Supportive care is provided to poisoned patient to keep the patient alive

until the physiological function is restored by further specific treatment.
Supportive care helps people meet the physical, practical, emotional and
spiritual challenges. It is done by monitoring the physiologic functions and
correct significant deviations from normal. During this course of action
anticipate and try to prevent complications.

Initial resuscitation should be based on the assessment of the patient and

not the particular toxin involved and standard advanced life support (ALS)
guidelines should be followed. Specific instances where treatment may
differ are indicated below. The majority of patients taking overdoses or
with drug toxicity are young and healthy, so cardiac and respiratory support
should be continued for much longer periods of time in patients with
toxicity-related cardiorespiratory arrest. If there is any doubt, cardiac
compression and ventillatory support should be continued until the
situation has been discussed with a clinical toxicologist. There has been
survival with normal neurological function in patients receiving
cardiopulmonary resuscitation (CPR) for hours.

As with any basic and advanced life support it is important to have a

systematic approach to managing toxicological emergency presentations.
Pioneers in the field developed RRSIDEAD as a mnemonic to remember the
key steps in patient assessment and management.

R – Resuscitation

R – Risk Assessment
S – Supportive Care

I – Investigations

D – Decontamination

E – Enhanced Elimination

A – Antidotes

D – Disposition

Some supportive cares are:

 Fluid therapy and feeding

 Analgesia, antiemetics and ADT (AAA)
 Sedation and Spontaneous breathing trial
 Thromboprophylaxis
 Head up position (30 degrees) if intubated
 Ulcer prophylaxis
 Glucose control
 Skin/ eye care and suctioning
 Indwelling catheter
 Nasogastric tube
 Bowel cares
 temperature control

A) AIRWAY:-

Monitoring and managing airways and breathing is crucial in the treatment

of poisoning. CNS depression is a common effect of drugs, so regular and
careful assessment of airway protection and patency is important. The
immediate need for assisted ventilation has to be assessed clinically, but
the efficiency of ventilation can only be gauged by measuring the blood
gases. Some drugs stimulate the respiratory centre. Eg. Amphetamines,
Atropine, Cocaine, and Salicylates. Some drugs are associated with non-
cardiogenic pulmonary oedema, characterised by severe hypoxaemia,
bilateral infiltrates on chest X-ray, and normal pulmonary capillary wedge
pressure. Eg. Calcium channel blockers, Anticoagulants, Beta-blockers, etc.
Some drugs cause or exacerbate asthma. The most important among them
include NSAIDs, antibiotics like penicillins, cephalosporins, tetracycline, and
nitrofurantoin, cholinergic drugs, chemotherapeutic drugs, and some
diuretics.

Management:

1. First establish an open airway:

• Remove dentures (if any).

• Use the chin lift and jaw thrust, to clear the airway obstructed by the
tongue falling back.
• Remove saliva, vomitus, blood, etc. from the oral cavity by suction or
finger-sweep method.
• Place the patient in a semi-prone (lateral) position. If required, insert an
endotracheal tube.
• If ventilation is not adequate, begin artificial respiration with Ambu bag.

2. Oxygen therapy:
This is done to raise the PaO2 to at least 45–55 mmHg (6.0 Kpa to 7.3 Kpa).
Begin with 28% oxygen mask. Depending on the response as assessed by
periodic arterial gas analysis, either continue with 28% or progress to 35%.
If the condition is relentlessly deteriorating, consider assisted ventilation.
B) Breathing:-
Toxicology patients rarely have hypoxia unless they develop aspiration
pneumonitis. The commonest problem is hypoventilation secondary to
respiratory depression Many people have problems with breathing and
shortness of breath. This can be a very upsetting symptom that can
significantly affect a person’s quality of life. People who are having difficulty
breathing and shortness of breath may also feel anxious.

Management:

Try different positions to find which ones help the patient breathe easier.
The patient can try sitting upright and leaning forward slightly and also try
using pillows to prop up head and upper body when they are sleeping.
Patient can try controlled breathing or pursed-lip breathing. Breathe in
slowly through nose, hold the breath for a few counts and then breathe out
through pursed lips like they are whistling. Patient can also try relaxation
exercises or meditation to help ease anxiety when you have trouble
breathing. Make patient sit near an open window or in front of a fan to get
extra air Opening a window or lowering the room temperature may also
help because cooler air is easier to breathe.

1)oxygen therapy

Oxygen therapy is a treatment that gives extra oxygen. It makes sure

patient gets enough oxygen if you have difficulty breathing. Patient breathe
the oxygen in through a mask over mouth or through tubes in the nostrils.
Oxygen therapy is usually only helpful if you have low levels of oxygen in
your blood (called hypoxemia).
2)Thoracentesis

Thoracentesis may be used to drain an abnormal buildup of fluid in the

space between the lungs and chest wall (called pleural effusion). The doctor
inserts a hollow needle through the skin into the space between the lungs
and the chest wall (called pleural cavity).

3) Paracentesis

Paracentesis may be used to drain an abnormal buildup of fluid in the

abdomen (called ascites). The doctor inserts a hollow needle or plastic tube
(called a catheter) through the skin into the abdomen. The doctor uses the
needle to drain extra fluid from the abdomen.

C) CIRCULATION:-

Common symptoms include alterations in mental status, an inability to

stand without dizziness, and/or severe generalized weakness. Physical
findings include pallor, cold clammy skin, gooseflesh, a thin or thready
pulse, an increased respiratory rate, tachycardia, and hypotension. In most
cases of death from acute poisoning, signs of acute circulatory failure were
observed at autopsy. Histological examination of the myocardium reveals
changes such as hyperaemia and extravasations in the stroma, and lesions
of the muscle fibres with the presence of a fuchsinophilic substance in the
myoplasm. Levels of potassium in the myocardium would be significantly
lower. Although the mechanisms, causes and clinical syndromes are
different the pathogenesis is the same, the circulatory system fails to
maintain the supply of oxygen and other nutrients to the tissues and to
remove the carbon dioxide and other metabolites from them. The failure
may be hypovolemic, distributive.

Management:

Inotropic support

The use of intravenous fluid therapy and inotropic support should be based
on patient haemodynamics and the specific toxins ingested. Although
specific inotropes or other drugs are suggested in toxicology patients, the
initial management of cardiogenic shock should be the same as for any
other cause unless there are specific contraindications to particular
inotropes.

The initial inotrope of choice is adrenaline unless its vasopressor actions are
contraindicated, such as in beta blocker overdose. Administration of an
inotrope should only be undertaken in consultation with a toxicologist or
cardiologist. Prolonged cardiopulmonary resuscitation is essential because
unlike in arrests due to cardiovascular disease, the majority of patients are
healthy prior to the overdose, and survival with normal neurological
function after long periods (hours) of cardiopulmonary resuscitation is well
documented.

Adult doses of Other inotropes used in toxicology -

a. Milrinone (phosphodiesterase inhibitor) :

 Milrinone 50 micrograms/kg IV, slowly over 10 minutes, followed by
0.375 to 0.75 micrograms/kg/minute IV, adjusting according to clinical
and haemodynamic response, up to a maximum of 1.13 mg/kg daily.

b)Insulin euglycaemia :
Short-acting insulin 1 unit/kg IV bolus, followed by 1 unit/kg/hour.
The dose can be increased to 2 units/kg/hour or further but this
should be discussed with a clinical toxicologist PLUS glucose 10% or
50% IV infusion.

D) SEDATION:-

Sedation is the reduction of irritability or agitation by administration of

sedative drugs, generally to facilitate a medical procedure or diagnostic
procedure. Drug induced sedation is also most common occurrence which is
generally unintended effects. Drugs in toxic doses can cause fatal
consequences of sedation. Examples of drugs which that cause sedation
include propofol, etomidate, ketamine, fentanyl, lorazepam and
midazolam. Airway obstruction, apnea and hypotension are not uncommon
during sedation and require the presence of health professionals who are
suitably trained to detect and manage these problems.

Management:

• If the patient feels drowsy and he needs to be monitored very closely.

Keep the patient away from areas of potential harm.
• If the patient wants to sleep, place them on their side with their chin up.
Wake your patient every now and then and encourage them to have
something to drink in order to prevent dehydration. At first it is best to give
the patient sips of clear liquids to prevent nausea.

• If the patient vomits, help them bend over and turn their head to the side
to insure that they do not inhale the vomit.

• Establish ABCs, obtain IV access, provide oxygen, and perform aggressive

supportive care with airway protection as necessary.

• Ensure adequate airway and ventilation. Consider and reassess the need
for endotracheal intubation.

E)SEIZURES:-

Seizures are a common complication of drug intoxication, and up to 9% of

status epilepticus cases are caused by a drug or poison. Basically, seizures
occur when our systems have reached this point of toxicity or overload,
even if the culprit drug is ecstasy, acid or heroin. While the specific drugs
associated with drug-induced seizures may vary by geography and change
over time, common reported causes include antidepressants, stimulants
and antihistamines. Seizures occur generally as a result of inadequate
inhibitory influences (e.g., gamma aminobutyric acid, GABA) or excessive
excitatory stimulation (e.g. glutamate) although many other
neurotransmitters play a role. Most drug-induced seizures are self-limited.
However, status epilepticus occurs in up to 10% of cases. Prolonged or
recurrent seizures can lead to serious complications and require vigorous
supportive care and anticonvulsant drugs. No characteristic clinical features
differentiate drug-induced seizures from idiopathic epileptic seizures. Use
of drugs known to cause seizures should be avoided in patients with
predisposition to seizu res.

Management:

• Initial treatment should include airway management with adequate

oxygenation and ventilation, stabilization of the blood pressure and heart

rate and rapid bedside testing of serum glucose concentration and core
body temperature.

• Gastric decontamination and enhanced elimination or antidote

administration may be appropriate in some patients, and consultation with
a medical toxicologist is recommended.

• Finger stick blood sugar, electrolyte imbalance and PH should be

monitored.

• Most drug-induced seizures resolve after discontinuation of the offending

drugs, but some patients require supplementary treatment, Eg, intravenous
diazepam.

• Benzodiazepines are generally accepted as the first line anticonvulsant

therapy for drug-induced seizures. If benzodiazepines fail to halt seizures
promptly,

• Continuous infusion of one or more anticonvulsants may be required in

refractory status epilepticus.
F) Renal dysfunction/Nephrotoxicity:-

Nephrotoxicity is toxicity in the kidneys. It is a poisonous effect of some

substances, both toxic chemicals and medications. There are various forms,
and some drugs may affect renal function in more than one way.
Nephrotoxins are substances displaying nephrotoxicity. Nephrotoxicity
should not be confused with the fact that some medications have a
predominantly renal excretion and need their dose adjusted for the
decreased renal function (e.g., heparin). The nephrotoxic effect of most
drugs is more profound in patients already suffering from kidney failure.
Nephrotoxicity is usually monitored through a simple blood test. A
decreased creatinine clearance indicates poor renal function. Normal
creatinine level is between 80 - 120 μmol/L. In interventional radiology, a
patient's creatinine clearance levels are all checked prior to a procedure.

Management:

Supportive care without dialysis focuses on relief from the discomfort and
pain of kidney failure symptoms, such as swelling and shortness of breath.

• Initial assessment begins with airway, breathing, and circulation

(A, B, C’s). Vital signs should be obtained, including blood
pressure.
• Patients should be placed on continuous monitoring and IV
access obtained. If acute kidney injury is suspected, evaluation
should be focused on life threatening complication of acute
kidney injury or renal failure
• Myoglobinuria can be treated by NaHCO3.
 • Anuria can be treated by administrating furosemide to block
tubuloglomerular feedback which causes constriction.
• Hyperkalaemia can be treated by sodium polystyrene sulfonate.

G) Drug induced Arrhythmias:-

QT prolongation and torsades de pointes: QT prolongation should be

monitored and any other precipitating factors should be determined and
treated if possible .Electrolytes including magnesium and calcium should be
checked and deficiencies corrected. Arrhythmia can be caused by both
cardiac and non cardiac drugs. Familiarity with these agents and their effect
on heart rhythm will keep you on the alert and allow you to anticipate
these adverse events before they arise. Patient with cardiac problems are
probably at higher risk.

Management:

Antiarrhythmic drugs can actually cause arrhythmias by affecting the

heart's potential while diuretics therapy can lead to arrhythmias by
upsetting electrolyte imbalance .This can be treated by following methods:

• Patients with Hypomagnesemia should have magnesium

replacement. Magnesium sulfate -50% 5 to 10 ml IV over
30 to 60 minutes.
• Patients with hypocalcaemia should have calcium replaced.
Calcium gluconate -10% 10 to 20 ml IV over 10 to 30 minutes.
• Patients with hypokalaemia should have potassium replaced.
 Potassium chloride -14 to 16 mmol orally, 3 times daily.
Or, potassium chloride -10 to 20 mmol IV over 1 to 2 hours.

• Isoprenaline or tranvenous pacing should be considered in

patients with a prolonged QT interval and Bradycardia.
Isoprenaline 20microgram IV, repeat the dose for clinical
response.
• Torsades de pointed may resolve spontaneously within a
minutes but if not then first line treatment is a 200 J DC or
equivalent. If there is no response DC shock is repeated with
increasing voltage shock. Magnesium should also be given.

References:
1) 1. ^ Schrager, TF (October 4, 2006). "What is Toxicology". Archived from
the original on March 10, 2007.

2. ^ Hodgson, Ernest (2010). A Textbook of Modern Toxicology. John Wiley

and Sons. p. 10. ISBN 978-0-470-46206-5.

3. ^ Levey, Martin (1966). Medieval Arabic Toxicology: The Book on Poisons

of ibn Wahshiyya and its Relation to Early Native American and Greek Texts.

4. www.PharmaDost.info