Beruflich Dokumente
Kultur Dokumente
Withdrawal
http://www.aafp.org/afp/2000/0501/p2763.html
An Approach to Drug Abuse, Intoxication and
Withdrawal
http://www.aafp.org/afp/2000/0501/p2763.html
Acetaminophen
• Recommended dosing 650-1000mg (adults) ; 10-
15mg in children, every 4-6 hours
• Max daily dose (adults) 4g; (children) 75mg/kg
• Complete absorption within 4 hours
Diagnosis
ACUTE CHRONIC
A single ingestion, Repeated supratherapeutic ingestion
occur within 8 hours & intentiona; occur >8hours
http://www.ijp-online.com/viewimage.asp?img=Indian%20J%20Pharmacol_2010_42_6_412_71894_u2.jpg
Treatment
• N-acetylcysteine
- Serves as a gluthathione (binding and detoxifying NAPQI and avoiding
subsequent hepatotoxicity
- Evident of hepatotoxicity NAC acts as a free radical scavenger & an
antioxidant and alters hepatic microcirculation and oxygen delivery
- In patients with acetaminophen-induced hepatic failure, IV
administration of NAC decreases the rates of cerebral edema,
hypotension, and death even when no acetaminophen remains
Opioid intoxication
• Opioid intoxication includes maladaptive behavioral
changes and specific physical symptoms of opioid
use
• Opioids refers broadly to all compounds related to
opium that possess analgesic and sedative
properties
• Opiate describes the opioid alkaloids found
naturally in the opium poppy plant, Papaver
somniferum
• Opioids most frequently involved in reported toxic
drug exposures were, in order of number of cases
recorded, tramadol, oxycodone, methadone,
morphine, buprenorphine, and hydrocodone
• Deaths were primarily associated with exposure to
methadone, oxycodone, and morphine
American Psychiatric Association. Diagnostic and statistical manual of mental disorders : DSM-5. 5th ed.
Opioid intoxication
TREATMENT
• Airway protection and ventilatory
maintenance are the most
important treatment steps for
opioid intoxications, because
respiratory depression is the
major morbidity and the cause of
essentially all the mortality
https://www.aclsmedicaltraining.com/bls-suspected-opioid-overdose-algorithm/
Opioid WITHDRAWAL
American Psychiatric Association. Diagnostic and statistical manual of mental disorders : DSM-5. 5th ed.
Opioid WITHDRAWAL
• Opioid withdrawal usually starts with feelings of
anxiety, yawning, lacrimation (TABLE 186-3)
• Onset of withdrawal is usually within 6 to 12
hours of last heroin use and within 30 hours of
last methadone exposure
• Symptoms of opioid withdrawal can be rendered
more tolerable by the administration of the
central α2-agonist clonidine, antiemetics, and
antidiarrheal agents
• Daily administration of a verified dose of
methadone PO (or half the verified dose IM if
the patient cannot take oral medications) is
recommended to inhibit withdrawal symptoms
and reduce craving
• Buprenorphine, 0.3 to 1.2 milligrams IV or IM
every 6 hours, can safely be administered to a
medically ill opioid-dependent patient
experiencing withdrawal who will be admitted to
the hospital
About two thirds of the body’s iron is incorporated into hemoglobin, and the
remainder is found in other iron-containing proteins such as myoglobin,
cytochromes, and other enzymes and cofactors, or is stored as ferritin.
The recommended daily intake of iron is about 8 milligrams for boys, adult
men, and nonmenstruating women; 18 milligrams for menstruating women;
and 27 milligrams for pregnant females.
Because excess iron is toxic, the body uses several mechanisms to maintain
iron homeostasis: serum protein binding, intracellular storage, and, most
importantly, regulation of GI tract absorption.
Iron is stored within the body in the form of ferritin, a large intracellular
storage protein that can reversibly bind as many as 4500 molecules of iron.
Ferritin can also be incorporated by phagolysosomes to form hemosiderin
granules.
Iron is a potent catalyst for the production of oxidants such as free radicals.
Iron is a direct GI tract irritant and causes vomiting, diarrhea, abdominal pain,
mucosal ulceration, and bleeding soon after a significant ingestion. As the
mucosal surface is injured, the regulatory enterocyte barrier is compromised,
and free iron passes unimpeded into the blood, becoming systemically
available.
Hepatotoxicity occurs as the portal blood supply delivers a large amount of iron to the
liver. In addition, coagulopathy unrelated to hepatotoxicity may occur through
inhibition of thrombin formation and the effect of thrombin on fibrinogen.
Five stages of clinical toxicity are traditionally described, although in more practical
terms, acute iron toxicity can be considered to manifest in two clinical stages: local GI
tract toxicity and systemic toxicity.
Stage 1
Is characterized by abdominal pain, vomiting, and diarrhea.
Iron is directly irritating and corrosive to the GI tract and typically induces vomiting within the
first few hours following ingestion.
Vomiting is the clinical sign most consistently associated with acute iron toxicity. Patients with
symptoms of gastric irritation may either recover over several hours or progress to systemic
toxicity.
The absence of GI symptoms within 6 hours of ingestion essentially excludes a significant iron
ingestion.
Stage 3
Is characterized by systemic toxicity from iron-induced disruption of cellular
metabolism with resultant shock and lactic acidosis.
Iron-induced coagulopathy may worsen bleeding and hypovolemia.
The coagulopathy may be biphasic, with prolonged prothrombin time and partial
thromboplastin time within the first 24 hours.
Tintinalli’s Emergency Medicine A Comprehensive Study Guide. 8th edition. 2016
Toxicology
Iron
This initial coagulopathy appears to be reversible with chelation therapy, because it
is free iron that initially interferes with the activity of factors in the coagulation
cascade.
Subsequent coagulopathy is from iron-induced hepatic injury that reduced
coagulation factor production.
During stage 3, renal failure, cardiomyopathy, and failure of other critical organ
systems may also occur.
Stage 5
Refers to delayed sequelae, including gastric outlet obstruction secondary to the
corrosive effects of iron on the pyloric mucosa.
Delayed sequelae are rare and occur 4 to 6 weeks after ingestion.
Tintinalli’s Emergency Medicine A Comprehensive Study Guide. 8th edition. 2016
Toxicology
Iron
Diagnosis
laboratory testing
Laboratory tests should include CBC, determination of serum electrolyte levels, renal
and liver function studies, coagulation function tests, serum glucose, and serum iron
levels, with the understanding that these results are to assess the overall condition of
the patient, because iron toxicity is largely a clinical diagnosis.
In general, serum iron levels measured within 4 to 6 hours after an acute ingestion
correlate with the severity of toxicity, but low serum iron levels do not necessarily
mean absence of toxicity.
Serum iron levels may be low because of variable times to peak level following
ingestions of different iron preparations, and treatment with deferoxamine can
artificially lower serum iron levels.
Serum total iron-binding capacity has little value in the assessment of iron-poisoned
patients.
It becomes falsely elevated in the presence of elevated serum iron levels or
deferoxamine, and significant organ damage occurs despite exceeding the serum
iron level.
Imaging
Standard ferrous sulfate tablets and reduced iron are radiopaque and frequently visible on
routine radiographs and this may help guide GI decontamination when present.
However, many iron preparations are not routinely detected, including pediatric chewable and
liquid preparations, and absence of radiopaque material on radiographs does not exclude iron
ingestion.
Patients with clinical toxicity should first be stabilized with attention to airway,
breathing, and circulation, after which GI decontamination and chelation therapy with
deferoxamine may proceed.
Patients with persistent vomiting and abnormal vital sign values or other signs of poor
perfusion or shock should undergo aggressive fluid resuscitation and treatment with
deferoxamine.
Coagulopathy should be treated with parenteral vitamin K and/or fresh frozen plasma,
as indicated.
Inorganic mercury salts are absorbed primarily through the GI tract, but
they may also be absorbed across intact skin. Mercuric salts deposit in the
ionized form primarily in the kidney, followed by the liver and spleen.
Mercury salts do not enter the CNS in consequential amounts nor do they
cross the placenta.
Inorganic and the aryl organic mercurials are eliminated in the urine and
feces. The short-chained alkyl compounds are excreted primarily in the bile,
where they undergo significant enterohepatic circulation.
Mercury binds with sulfhydryl groups, affecting a diverse number of enzyme and
protein systems.
Methyl mercury also inhibits choline acetyl transferase, which catalyzes the final step
in the production of acetylcholine and may produce symptoms of acetylcholine
deficiency.
The clinical effects of mercury poisoning depend on the form and, in some cases, the
route of administration. In general, the neurologic, GI, and renal systems are
predominantly affected.
Elemental Mercury
Acute symptoms following inhalation of elemental mercury vapor include shortness of breath,
fever/chills, cough, nausea, vomiting, diarrhea, metallic taste, headaches, weakness, and blurry
vision.
In severe cases, patients may develop acute lung injury and severe respiratory distress.
Following metabolism of ingested or injected elemental mercury to inorganic salts, patients
may also develop signs of inorganic mercury toxicity, including tremor and renal failure.
Inorganic Mercury
Mercury salts are caustic, and an acute ingestion produces a severe hemorrhagic gastroenteritis
with abdominal pain often associated with a characteristic graying of the oral mucosa and
metallic taste.
Shock and cardiovascular collapse may rapidly ensue.
Acute kidney injury results from both direct toxicity of the mercury ions and from decreased
renal perfusion due to shock.
GI symptoms of chronic inorganic mercury toxicity include metallic taste, burning sensation in
the mouth, loose teeth, mucosal lesions and fissures, excessive salivation, and nausea.
Hallmarks of chronic neurologic toxicity include tremor, neurasthenia, and erethism.
Neurasthenia is characterized by fatigue, depression, headaches, and difficulty concentrating.
Erethism refers to behavioral changes characterized by shyness, emotional lability, irritability,
insomnia, and delirium.
Chronic renal toxicity ranges from reversible proteinuria to the nephrotic syndrome.
Organic Mercury
The short-chained alkyl compounds, methyl, dimethyl, and ethyl mercury, have the
most devastating effects on the CNS.
After a latent period of weeks to months, orofacial paresthesias are a common initial
symptom, followed by headache, tremor, and fatigue. In severe cases, patients may
develop ataxia, muscle rigidity and spasticity, blindness, hearing deficits, and
dementia.
Although less prominent than the neurotoxicity, mild GI, renal, and pulmonary
abnormalities may develop with organic mercury poisoning.
Ingestion of mercuric chloride can produce a rapidly fatal course and should be
considered in a patient presenting with a corrosive gastroenteritis.
Often, however, the diagnosis of mercury toxicity is subtle, arrived at only after many
other diagnoses have been investigated.
For poisoning from all forms of mercury, except short-chained alkyls, a 24-hour urinary
measurement of mercury should be performed after a 5-day seafood-free diet.
A seafood meal (contaminated with mercury) can temporarily elevate the mercury
level to the toxic range until the mercury is eliminated. Most unexposed individuals
will have 24-hour urine mercury levels <10 to 15 micrograms/L (<0.05 to 0.075
micromol/L).
Although elevated blood or urine values are necessary to confirm the diagnosis, they
correlate poorly with toxicity and are unable to distinguish the asymptomatic exposure
from mercury poisoning.
Hemodialysis does not enhance mercury clearance but may be indicated for
treatment of acute kidney injury.
American Psychiatric Association. Diagnostic and statistical manual of mental disorders : DSM-5. 5th ed.
ALCOHOL WITHDRAWAL
• TIMELINE ALCOHOL WITHDRAWAL SIGNS AND SYMPTOMS
• Alcohol withdrawal syndrome can occur as early as 6 hours after alcohol cessation,
usually peaks after 2-3 days, and can persist up to 7days after alcohol cessation