Emergencies

American Manual
of Examination
in Medicine
(2CK)

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Emergencies

American Manual
of Examination
in Medicine
(2CK)
Author

Luis Cabeza Osorio

A m e r i c a n Manua l o f Ex am i na ti o n i n Me di c ine (2CK)

Index
01. Initial Treatment
of Polytraumatized Patient ......................................................... 1
1.1. Advanced Trauma Life Support
Recommendations.............................................................................................................. 1

02. Shock........................................................................................................................ 2
2.1. Types of Shock........................................................................................................................... 2

04. Abdominal Trauma............................................................................... 3

4.1. Blunt Abdominal Trauma........................................................................................... 4
4.2. Open Abdominal Trauma ........................................................................................ 4

05. Acute Appendicitis ............................................................................... 4

06. Postoperative Fever ............................................................................ 5

03. Chest Trauma................................................................................................ 3

3.1. Open Pneumothorax ....................................................................................................... 3
3.2. Tension Pneumothorax ................................................................................................ 3
3.3. Flail Chest or Unstable Thorax .......................................................................... 3

07. Burns ......................................................................................................................... 6

08. Toxicologic Emergencies ............................................................ 7

Em e rge ncies

Initial Treatment
Chapter 01

of Polytraumatized
Patient

A patient is considered polytraumatized when they present two or more

serious traumatic injuries peripheral or visceral) that negatively impact
one or more of their vital functions, threatening survival.
Traumas are the most frequent cause of death among the 1 to 45 yearold age group. Most polytraumatized patients are a consequence of
trac accidents.
Death is produced in three peaks:
Immediate: seconds or minutes: because of apnea, obstruction of
the airway, or massive hemorrhaging. Only preventive measures
may be employed.
Early: minutes or hours: because of hypovolaemia, cerebral lesions
or respiriatory failure. Diminished with correct early polytrauma
care (ABCDE).
Later stage: days or weeks: because of sepsis, multiorgan failure,
res-piratory distress, brain damage, etc. Also influenced by initial
care along with identification of injuries.
Initial care for a polytraumatized patient must be performed following
two basic principals:
1. Injuries should be treated in order of importance: those which are
life threatening must be treated first.
2. The lack of a definitive diagnosis should not impede adequate
treatment.

1.1. Advanced Trauma

Life Support (ATLS)

Recommendations

Breathing (respiration and ventilation)

When presented with respiratory distress, the following must be ruled
out:
Tension pneumothorax.
Open pneumothorax: exit of air through the wound.
Flail chest.

Circulation
Circulation (assessment and treatment of the state of shock with control of actively bleeding points). The hemodynamic status may be determined by the patients state: level of conciousness, coloring, pulse
(tachycardia + chill = hypovolemic shock).
Treatment is focused on two points:
Control of hemorrhaging.
Volume replenishment. Hypertension in the polytraumatized patient is hypovolemic until shown otherwise, and this requires that at
least two peripheral venous lines be inserted and that 2,000 mL of
serum be quickly administered.
If the patient does not respond to the treatment with volume, it is necessary to evaluate the administration of blood (always requesting crossmatch) and look for other non-hemorrhage causes of shock: myocardial
dysfunction, tension pneumothorax, neurogenic (hypertension without
tachycardia) and in rare cases, sepsis.

Disability
Disability (neurologic injury). The objective is to detect the neurologic
disturbance requiring immediate emergency treatment. The exploration consists of evaluating consciousness level using the Glasgow
coma scale (see the Section Neurology and Neurosurgery) and the examination of pupillary reflex response. A consciousness level that has
dropped to a Glasgow of 8 or below justifies intubation and mechanical
ventilation.
In order to avoid brain damage in a patient with craniocerebral trauma,
correct A, B, C must be maintained (ensuring the airway, good oxygen
flow and normovolemia).
Hypertension is never because of brain damage (except in terminal cases).

This initial management should be carried out in five dierentiated

phases, according to the American College of Surgeons (ATLS).

Airway + protection of the cervical spine

Extraction of foreign bodies and elevation of the chin with anterior jaw
thrust. Guedel airway, with case arrived, intubation (Table 1).

Inadequate ventilation or oxygen

Glasgow < 8, or requiring transfer
Wounds to neck or face that threaten permeability of airway
Multiple serious injuries
Serious shock
Agitated patients

Exposure/Environmental
Consists of the complete exposure of the patient, undressing them
and turning them over, as well as the prevention of hypothermia. The
patient must be reheated using a thermal blanket and the infusion of
warm serum, in order to prevent the fatal triad: hypothermia, acidosis
and coagulopathy (Table 2).

A. PERMEABLE AIRWAY AND CERVICAL SPINE

Oxygen
Cleaning and maintenance
of airway (Guedel intubation)
Neck brace

Table 1. Recommendations for orotracheal intubation

Table 2. Summary of Phase I with supplementary measures at rst

(with cervical protection)

recognition (continue)

A m e r i c a n Manua l o f Ex am i na ti o n i n Me di c ine (2CK)

B. VENTILATION
Insufficient respiratory value
Intubation and mechanical
ventilation
Rule out: tension pneumothorax,
massive hemothorax,
intrathoracic drainage

Rx chest and cervical spine

(portable)
Oxygen mask
Oxygen measurement

OBSTRUCTIVE SHOCK

Diaphoresis

C. CIRCULATION
Control of external hemorrhaging
Volume replenishment (shock
control): 2 L Ringer lactate
Look for internal hemorrhaging:
abdomen, chest, pelvis,
retroperitoneum, extremities
Assess other causes of shock

HYPOVOLEMIC SHOCK

Pneumothorax

Vomiting

Two periphery openings +

analytics: crossmatch, toxicity,
pregnancy tests
Eco-fast, peritoneal cleansing
ECG
Pelvis Rx
Urinary catheterization (if no
fracture, rectal exam previous)
Nasogastric tube

Burns

Pulmonary embolism
Blockage

Hemorrhage

CARDIAC SHOCK

D. NEUROLOGICAL EXAMINATION
Pupils
Glasgow
E. EXPOSURE
Prevention of hypothermia

Warm serum
Thermal blanket

DISTRIBUTIVE SHOCK

Table 2. Summary of Phase I with supplementary measures

Intense internal
urine output

at rst recognition (continued)

Shock

Figure 1. Types of shock

Chapter 02

Intrinsic cardiogenic shock: caused by the drop in cardiac output associated with the loss of systo-diastolic cardiac function.
The most frequent cause is an extensive acute myocardial infarction.

See Table 3.

TYPES OF SHOCK

PVC

GC

% SAT O2
VENOUS

RVP

Hypovolemic

Cardiogenic

Obstructive

Septic

Hyperdynamic

Hypodynamic

Neurogenic

Anaphylactic

Tabla 3. Hemodynamic parameters in dierent types of shock

2.1. Types of Shock

(Figure 1)

Hypovolemic: is most frequent. This is produced by a decrease in

the volume of blood available within vessels, whether because of
evident or occult hemorrhaging, dehydration.

Extracardiac cardiogenic or obstructive/compressive: because of

extrinsic pressure on heart chambers leading to a diastolic failure of
the heart, as occurs with pericardial tamponade, tension pneumothorax, large diaphragmatic hernias, mechanical ventilation, massive pulmunary embolism, etc.
Distributive: characterized by a generally high cardiac output,
but with a poor distribution thereof. The most frequent sub-type
is septic shock, which typically appears in the elderly, those with
suppressed immune systems or patients subjected to invasive
procedures or surgery, in relation to infections (primarily lung,
abdominal or urogentinal in nature). On occasion, especially
virulent pathogens, such as meningococcus, may be produced
in previously healthy patients. Septic shock may present two
hemodynamic patterns according to the point of evolution: one
initial or hyperdynamic and another in advanced phases, hypodynamic.
Treatment is aimed at correcting the specific triggering cause, associated with general measures of vital support based upon the clinical situation (assisted breathing, blood volume replacement, vasoactive drugs,
antibiotics, etc.).

Em e rge ncies

Chest Trauma

3.3. Flail Chest or Unstable

Thorax

Chapter 03

3.1. Open Pneumothorax

Consequence of an injury penetrating the chest. Air enters the thorax
more easily upon inhalation than when exhaling, which creates progressive collapse of the lung. During inhalation, the mediastinum is
pushed towards the healthy side and during exhalation, towards the
injured side, producing a mediastinal swaying that decreases venous
return, and, as a consequence, cardiac output. It tends to be associated
with lung injury.

This is because of a double fracture in three or more adjoining levels.

This creates a floating central portion in the chest wall that oscillates
with respiration in a way inverse to or counter the rest of the wall. The
most important factor is not the damage to the wall but rather the associated injuries: lung contusion (which causes respiratory failure), hemothorax and pneumothorax.
For treatment, the first step is analgesia, which enables chest physiotherapy, and secondly, the control of respiratory function (Figure 3).

The first emergency measure consists of restoring the integrity of the

chest wall using a dressing applied to three points (valvular eect) and
the placement of intrathoracic drainage far from the point of injury. This
is followed by definitive closure.
Inhalation

3.2. Tension Pneumothorax

If there is clinical suspicion (absence of vesicular murmur, lack of chest
movement, contralateral tracheal deviation and jugular engorgement,
with respiriatory failure) with need for radiologic verification immediate decompression must be performed with a large needle in the 2nd
intercoastal space medioclavicular line (Figure 2).

Exhalation

Figure 3. Flail chest

Abdominal
Chapter 04

Trauma

Initial care of the polytraumatized patient must be addressed by priorities in a way which is fast, clear and sequential.

Figure 2. Tension pneumothorax: collapse of the right lung with

deviation of mediastinum to the left

A protocol known as ATLS (Advanced Trauma Life Support) has been

established, which consists of a rapid first check, with resuscitation and
the restoration of vital functions:
A. (Airway). Maintenance of the airway with control of the cervical
spine.
B. (Breathing). Breathing and ventilation.
C. (Circulation). Circulation with control of hemorrhages (Table 4).
D. (Disability). Neurologic deficit.
E. (Exposure/Environmental). Exposure: undress the patient completely and prevent hypothermia.

A m e r i c a n Manua l o f Ex am i na ti o n i n Me di c ine (2CK)

Vascular filling
State of consciousness
Pulse (cardiac frequency) and BP (blood
ASSESSMENT
pressure)
Urine output
Cardiac auscultation
ECG Monitoring
Bleeding external injuries: compression
CONTROL OF
Closed abdominal trauma/pelvic injuries
HEMORRHAGING
(surgery/arteriography)
Analytics and crossmatch
VENOUS ACCESS
Resuscitation with fluids
Table 4. Assessment and actions during circulatory evaluation

4.1. Blunt Abdominal Trauma

LAPAROSCOPY DIAGNOSIS
Technique

Optimal trocar generally umbilical

Recommendations

Above all with open trauma injuries

Patients with stab wounds in the anterior and
lateral abdominal wall
Chest/abdominal trauma with suspected
diaphragmatic injury
In order to assess possible peritoneal
penetration
Tangential firearm wounds in the lower chest
Possible need for surgical intervention

Advantages

Reduces blank laparotomies

Lower mortality
Less time in hospital

Disadvantages

Does not enable detection of injury in hollow

viscera or retroperitoneum

Table 5. Laparoscopy in abdominal trauma

4.2. Open Abdominal Trauma

CLINICAL CRITERIA

RADIOLOGIC
CRITERIA

1. Closed abdominal trauma with positive eco

Fast or PLPD and hemodynamic instability
2. Signs of peritonitis
3. Closed abdominal injury with adequate
resuscitation in which new hypotension appears
4. Hypotension in patient with penetrating
abdominal injury
5. High or low gastrointestinal or genito-urinary
bleeding with penetrating injury
6. Firearm wound that cuts through
the vascular or visceral peritoneal
or retroperitoneum cavity
7. Evisceration
1. Pneumoperitoneum
2. Pneumoretroperitoneum
3. Radiologic findings (CT) of injury in hollow
viscera
4. Injury to the urinary bladder determined in CT
5. Injury to the renal pedicle vessel diagnosed
by CT
6. Severe injury to solid organs diagnosed
by CT, in not candidates for a conservative
management

Table 6. Recommendations for emergency surgery in abdominal trauma

Acute Appendicitis
Chapter 05

Acute abdomen frequently requiring surgery. Mortality in cases not presenting complications is approximately 0.3%, increasing to 3% in the
case of perforation and reaching 5%-15% among the elderly population.
In general, with correct anamnesis and with examination data gathered
in a search for signs of peritoneal irritation in the right iliac fossa (RIF),
in a typical patient this is sucient for diagnosis and surgical indication (Table 7).

CATARRHAL
OR MUCUS
PHLEGMONOUS
PURULENT
GANGRENOUS

Oral submucus inflammation. Macroscopically

normal
Mucus ulceration
Purulent extrusion (light and perpendicular)
Necrosis and perforation
Localized/confined peritonitis
Diffuse peritonitis

Table 7. Types of appendicitis

Physical Examination
The objective of abdominal examination is to determine the exact location of the pain and evidence of the peritoneal irritation. Pain upon
probing the RIF, or the McBurney point (located at the meeting point of
the two medial thirds with the lateral third of an imaginary line joining
the navel with the right anterior superior iliac spine).
The characteristic signs of peritoneal irritation in acute appendicitis are:
Blumberg sign: pain in RIF triggered by sharp pressure applied to the
McBurney point.
Rovsing sign: pain in RIF triggered by deep pressure or tapping on
the left iliac fosse.
Psoas sign: pain in RIF caused by the active flexing or passive extension of the ipsilateral hip. Indicates that the location of the appendix
is retrocecal.
Shutter sign: Pain upon internal hip rotation with the knee flexed.
This is associated with an appendix located in the pelvis.

Complementary Laboratory Exams

Blood count: leukocytosis and neutrophilia.
C-reactive protein (CRP): tends to be elevated, particularly in cases
whose clinical course is further advanced.

Radiology
Patients with typical symptoms and the concurring analytics, above all
if they are young males, can be treated for acute appendicitis without
need for imaging tests.
Abdominal ultrasound (US): ultrasound and abdominal CT scan are
suitable tests to study a patient with acute appendicitis. In spite of its

Em e rge ncies

lesser sensitivity, ultrasound is considered the image test of choice (Figures 4 and 5 and Table 8).

3/3
2/3

1/3

Incision

Figure 4. Ultrasound of acute appendicitis

Figure 6. Incision for appendectomy

Vomit. Vomiting is of greater value following the first trimester since

in the first trimester it may be confused with gravidarum emesis
Fever: fever may be absent in the pregnant woman
Tachycardia: Does not change with pregnancy. When above
120/minute, suspect complications
Diarrhea or constipation

Table 8. Clinical case typical of pregnant woman with appendicitis

Postoperative
Chapter 06

Fever

Treatment
Treatment must adapt to the dierent clinical situations and the point
of evolution. This is based upon three key elements:
1. Elimination of the principal septic point by means of an appendectomy
(Figure 6).
2. Appropriate antibiotic therapy: prophylactic, and in some cases,
therapeutic.
3. Monitoring of evolving complications and of recurrence.

A common complication during the postoperative period. The causes

may be infectious or non-infectious. The time at which the operationrelated fever appears helps to focus the diagnosis (Figure 7):
Inter-operative or immediate postoperative period. May result
from a pre-existing infection, intra-operative handling of purulent
material, transfusion reaction, adverse reaction to medications or
malignant hyperthermia.

Suspicion of appendicitis

Clinical history analytical physical

exam abdominal ultrasound

Confirmed

Doubtful

Rejected
Look for other
etiologies

Surgery

Emergency room
observation

Abdominal TC

Confirmed
Repeat US and analysis
and reassess
in a few hours

Surgery

Not confirmed

Look for other

etiologies

Observations vs
laparoscopy diagnosis

Figure 5. Diagnosis and treatment of acute appendicitis

A m e r i c a n Manua l o f Ex am i na ti o n i n Me di c ine (2CK)

First 24 hours of the postoperative period. In the absence of a preexisting infection, atelectasis is the most frequent cause.
24 to 72 hours following the postoperative period. Usually attributed to respiratory complications or phlebitis in the veins used to
insert catheters.
More than 72 hours after the postoperative period. The existence
of fever after the third postoperative (p.o.) day or a fever that persists more than two days p.o. is suggestive of an infectious cause
(urinary, infection of the surgical wound, intra-abdominal abscess)
or deep vein thrombosis.

Burns
Chapter 07

According to the Causal Agent

Thermal: primarily accidents in the home.
Electric: short circuit and passage of electrical current.
Chemical: with acid or alkali.
The seriousness of the burn is determined by the type of causal agent, the
time of exposure and the temperature, and is quantified based upon the
characteristics of the patient, the area aected and its extension and depth.

START OF FEVER

For both sexes, the most common burn location is in the upper extremities.
Inter-operatory
or immediately
postoperative
Preoperative
infection
Transfusion
reaction
Management
of purulent
cavities

First 24 hours

24-72 hours

Following 3 days

Atelectasis,
infection-wound
from group A
anaerobics
or streptococcus

Septic phlebitis
(catheters),
pneumonia

Infectious: surgical
wound, UTI*, intra
abdominal abscess
(fistulas, leaks)
DVT**

Diagnosis
Extension: see Figure 8.
Depth: clinical diagnosis based upon appearance and vascular filling; grade based upon the penetration in the skins layers (Figure 9
and Table 9).

Treatment

* UTI: Urinary tract infection

**DVT: deep vein thrombosis

Figure 7. Start of fever

Initial management: ATLS protocol:

Airway with monitoring of the cervical spine.
Ventilation.
Circulation.
Neurologic deficit.
Exposure with monitoring of room temperature.
Fluid resuscitation.

Figure 8. Lund and Browder Diagram

Em e rge ncies

CONVERSE-SMITH
First degree

ABA DENOMINATION
Epidermic

HISTOLOGIC LEVEL
Epidermis

Second degree superficial

Dermal superficial

Epidermis and papillary dermis

Second degree deep

Dermal deep

Third degree

Total thickness

Epidermis and papillary dermis

and reticulate. Affects hair and
some vessels
Epidermis, dermis and hypodermis
(subcutaneous cellular tissue), and
may even reach the bone level

PROGNOSIS
Graft not necessary. Should heal on
its own in 7 days, without further
complications
Should heal over spontaneously in 15
days with some esthetic marks.
If complications arise, it may deepen
Normally requires grafting because of
esthetic and/or functional consequences.
May require tangential sclerectomy
Requires early sclerectomy, and grafts or
flaps

Table 9. Classications of burns and prognosis implications

Healing: in operating room and under sterile conditions. Routine antibiotic prophylaxis treatment is not recommended.
Surgical:
Scarectomy: Consists of removal of the necrotic or devitalized
tissue; within the first 48 hours; recommended in case of third
degree and deep second degree burns.
Skin grafts and flaps (Figure 10).

Figure 9. Second and third degree burns on a hand

Toxicologic
Chapter 08

Emergencies

See Tables 10, 11, 12 and 13.

TOXIN
Tricyclic antidepressants
Barbiturates
Benzodiazepines
Beta-blockers

Ca antagonists

CLINICAL ACTION
Anticholinergic**
Sympathomimetic**
Coma, miosis, hypotonia
Drowsiness, stupor, coma, ataxia,
normal pupils, hypoventilation
Bradycardia, AV block. QRS width,
hypotension, hypoglycemia,
seizures, coma
Bradycardia, arrhythmia,
hypotension, seizures, lethargy,
coma, shock

Figure 10. Skin autograft following deep second degree scald burns
in the distal region of both lower legs and the dorsal area of both feet.
In the upper part of the image, the donor area of healthy skin can be
seen at the level of the left thigh
ANTIDOTE / TREATMENT
Physostigmine
Forced alkaline diuresis
Flumazenil (0.5 mg i.v./2 min
to 2-3 mg)
Glucagon Isoprotesenol
(1-3 mg /1min. Next: 5 amp
at 250 cm3/50-100 mL/h + anti-emetic)
Chloride / calcium carbonate 10%
(5-10 mL i.v./i.v. slow 10-30)

OTHERS
ECG monitoring
No digoxin if arrhythmia
ECG + Rx Chest
Severity: depends on age
Respiratory distress in severe
asthma
Atropine if HR < 40 bpm

Table 10. Summary of main acute toxins (continued)

A m e r i c a n Manua l o f Ex am i na ti o n i n Me di c ine (2CK)

TOXIN

CLINICAL ACTION

ANTIDOTE / TREATMENT

Digital kneading

Asthenia, nausea, vomiting,

diarrhea, AV block, shortened QT,
ESV*

Digitalis antidot BM, atropine,

lidocaine (TV)/verapamil (TSV)

Extra cardiac clinical: earlier.

Correlation K+ and mortality!

Neuroleptics

Drowsiness, lethargy, ataxia,

lengthened QT and QRS,
hypotension

Biperiden/diazepam
(5 mg/30 min to 20 mg/10 mg)

Neuroleptic malignant syndrome:

Dantrolene (10 mg/kg/i.v.)

Lito

Neurologic, digestive, cardiac

Hemodialysis

Activated charcoal is not indicated

Paracetamol

Toxic dose: 10-15 g

Lethal: 15-25 g

N-acetylcysteine (choice < 8 h

helpful to 36 h)

Monitor liver function

Coagulopathy + encephalopathy:
ICU

Salicylates

Mild: nausea, vomiting, tinnitus

Moderate: vertigo, hypercapnia
Severe: confusion, convulsion,
coma

Forced alkaline diuresis

Mild: < 150 mg/kg

Moderate: 10 g
Severe: 20 g

Amphetamines

Hyperactivity, tachycardia,
dehydration, bruxism

Gastric lavage + activated

carbon
Acid forced diuresis

Acute psychosis
Malignant hyperthermia

MDA

Euphoria, hallucinations,
confusion, anxiety, tachycardia,
arrhythmias

Treatment support/symptoms
(Benzodiazepines/neuroleptics)

Bad trips, flashbacks

Mandibular movements

MDMA

Euphoria, hallucinations,
confusion, anxiety, tachycardia,
arrhythmias

Treatment support/symptoms
(Benzodiazepines/neuroleptics)

Bad trips, flashbacks

Mandibular movements

Ketamine

Euphoria, hallucinations, confusion Support treatment

Bad trips, flashbacks

Cocaine

Euphoria, seizures, psychosis,

arrhythmias

Diazepam/propranolol (10-20 mg
p.o./1 amp 5 mg)

Never administer lidocaine

Ethanol

Incoordination, dysarthria,
diplopia, euphoria, lethargy,
aggression, coma

Thiamine (100 mg. i.v.) + SG 5% +

B6 (4 amp in 500 cm2/8 hour)

Enol fetor

Liquid Ecstasy

Euphoria, excitement, delirium

Support treatment

Small increase in dose: significant

poisoning

Opiates

Miosis, analgesia, sedation,

respiratory depression,
constipation

Naloxone (0.4 mg i.v. + 1-2 mg/5

min if required)
Thioamide 100 mg i.v.

Overdose
Withdrawal
Unit

Cannabis

Hallucinations, tachycardia,
conjunctival hyperemia, mucosal
dryness

Diazepam/dipotassium
clorazepate (v.o. or i.m: in the case
of panic attack)

Chronic use: pulmonary

complications

Poppers

Dizziness, headache, tachycardia,

Methylene blue (1.2 mg/kg in 100
palpitations, hypotension, cyanosis mL SG 5%)

Avoid sildenafil

Burundanga

Anticholinergic

Assault drug

Peyote

Euphoria, hallucinations, mydriasis, Support treatment/symptoms

tachycardia, tremor

Bad experience bad trips, feel

good

LSD

Euphoria, hallucinations, delusions, Support treatment/symptoms

mydriasis, tachycardia, tremor

Bad trips

Toluene

CNS depression, arrhythmias,

pharyngitis, conjunctivitis, nausea

Respiratory assistance. If oral

ingestion: gastric lavage

Glue and solvent sniffers

Caustics

Sore throat, esophageal, salivation,

hematemesis, stridor, hoarseness

RX/thorax/abdomen,
Early endoscopy

Do not wash with SNG, do not

induce vomiting or neutralize

Ethylene

Abdominal pain, seizures, agitation Pyridoxine/thiamine/ethanol

(100 mg/100 mg)

Very specific hearing loss

Physostigmine

Table 10. Summary of main acute toxins (continue)

OTHERS

Ingesting of photocopier toner

Ingesting of antifreeze

Em e rge ncies

TOXIN

CLINICAL ACTION

Methanol

Blindness, abdominal pain,

agitation, seizures

Organochlorine

Anticholinergic**

Organophosphates

Hypersalivation,
anticholinergics**

Carbamates
Herbicides
Lead

Anticholinergic**
Coagulopathy
Abdominal pain (lead colic)
Encephalopathy
GEA*
Hemorrhagic colitis stomatitis
Digestive and respiratory clinic

Mercury
Arsenic
Carbon monoxide
Cyanide
Irritants
Smoke
Mushrooms

ANTIDOTE / TREATMENT
3

OTHERS

Ethanol (i.v. or 50 cm orally)

Fomepizole (1g/kg: maintenance
10 g/h)
Folinic-acid (50 mg slow i.v.)
Gastric lavage and activated
charcoal
Atropine (2 mg i.v.; repeat every
10 min)
Pralidoxime (1g in 100 mL of SSF)

Agricultural products; do not

administer adrenaline

Atropine (for 12 h)
Vitamin K (1 ampoule/8h)
Dimercaprol (4 mg/kg i.m.)

Fresh plasma if active bleeding

Bruxism in gums

Dimercaprol (4 mg/kg/4 h i.m.)

Behavioral changes (chronic)

Dimercaprol (4 mg/kg i.m.)

Fumes
Oxygen 100%
Hydroxocobalamin
(5 g i.v. in 10 min)

Hypoxia. Lactic Acid

Hyperventilation.
Glottis edema. Asfixia. Seizure.
Symptomatic
Cough. Dyspnea. Stridor. Edema
Symptomatic
Mushrooms
Cholinergic syndrome**
Atropine syndrome**
Gastroenteritis
Hepatonecrosis
Renal failure

Ingesting of antifreeze
Ingesting of varnish

Dermatitis in chronic intoxication

Skin: cherry red color
Typical: bitter almond odor
Very lethal
Blackish phlegm

Amanita phalloides

Cortinarius orellanus

Tubulo-interstitium nephritis

Symptomatic. Renal function

support

Late onset

Amanita muscaria

Abdominal pain
Anticholinergic syndrome**

Benzodiazepine
Physostigmine (1 mg i.v.)

Early onset

Entoloma lividum

Gastroenteritis

Symptomatic

Early onset

Atropine. Physostigmine

Watch hepatotoxicity

Vitamin K (1 cm 3/12 hours)

Ondansetron (8 mg i.v.)
Activated carbon

Aspirate with SNG

Evaluate hemodialysis
Late onset

* VES: ventricular extrasystoles. VT: ventricular tachycardia. SVT: supraventricular tachycardia. AG: acute gastroenteritis
** Summary of key toxicological symptoms

Table 10. Summary of main acute toxins

CHOLINERGIC
ANTICHOLINERGIC

Miosis, bradycardia, vomiting, diarrhea,

lacrimation, sphincter relaxation
Mydriasis, tachycardia, dry mucus membranes,
thirst, delirium

SYMPATHOMIMETIC HTA tachycardia, agitation

NARCOTIC

Punctate miosis, central depression,

hypotension

Table 11. Summary of main acute poisonings

SEVERITY
ACCORDING TO CO
LEVELS IN BLOOD
Mild (15-25%)

Nausea. Vomiting. Dizziness. Headache

Moderate (25-40%)

Dyspnea. Confusion. Cyanosis. ECG abnormality

Severe (40-60%)

Myalgia. Hypertonia. Tremor. Convulsions.

Skin/mucus: cherry red color.
Poor prognosis
Cardiorespiratory arrest. Death

Critical (> 60%)

CLINICAL MANIFESTATIONS

Table 13. Carbon monoxide poisoning (CO): symptomatology

TIME AFTER INTAKE
24 hours
24-72 hours

CLINICAL MANIFESTATIONS

N- ACETYLCYSTEINE (NAC)

Asymptomatic. Nausea. Vomiting.

NAc orally (diluted in juice):

MEG. Profuse sweating

150 mg/kg + 70 mg/kg every 4 hours until 17 doses

RH* pain. Hypertransaminasemia.

Intravenous NAC: 150 mg/kg

Coagulopathy. Jaundice. Renal complications. Cytopenias

In 250 mL of GS at 5% (1 hour) + 50 mg/kg

In 500 mL of GS at 5% (4h) +

72 hours - 5 days

Hypotension. Shock. Fulminant liver failure

100 mg/kg in 500 mL of SG at 5% (16 h)

Renal HD if > persists 48 hours. Transplant if liver failure appears.

* RH: right hypochondrium HD: hemodialysis. GS: glucose serum

Table 12. Top toxicological symptoms