Day 3

I. Medication
Medication list that is given in methodical materials is taken from “ the List of Recommended
Medicines and Equipment of the International Medical Guide for Ships 3rd edition, pages 430-
461 and the First Aid Kit , page 432” that provide recommended minimal of medication on
board and can differ from advanced medication kit on vessels.
https://lagaay.com/assets-frontend/flags/IMGS1_2009.pdf
There are different routes of administration, that is mentioned on a package of medication.
Main abbreviations:
i.c – intracutaneous (epidermal injection)
s.c. – subcutaneous (dermal injection)
i.m. – intramusculare (muscular injection)
i.v. – intravenosae (venous injection) . Medication should be diluted (NaCl 0,9% or similar)
before administration
p.o – per os (medication is given by mouth)
s.l. – sublinguale (medication is given under the tongue)
p.r – per recti (medication is given rectal)
List of recommended medication on board:
1. Antibiotics
Antibiotics are medicines that help stop infections caused by bacteria. They do this by killing the
bacteria or by keeping them from copying themselves or reproducing. The full course of
antibiotics should be given (7-14 days) to prevent bacterial assimilation and resistance creation
to antibiotics. If antibiotics is ineffective (no effect in 72 hours of administration) – medication
should be changed for a different group of antibiotics.
Amoxicillin + clavulanate tablet 875mg/125mg
Azithromycin tablet 500mg
Ceftriaxone ampoule 1g powder for injection (dissolve in water for injection)
Ciprofloxacin tablet 250mg
Doxycycline tablet 100mg
Metronidazole tablet 500mg
Tetracycline 1% ointment ointment 5 g (to treat minor eye infections; to prevent infections
following damage to the cornea)

2. Analgesics
Medications producing diminished sensation to pain without loss of consciousness: a drug that is
used to relieve pain and produce analgesia:
• opioid analgesics – medications should be administered under control to prevent
overdose
• a topical analgesic
 • NSAIDS – medication administration can cause internal bleeding (gastroduodenal ulcer
bleeding etc.) Not recommended to use medication on empty stomach as well as
overdosating medication in case of severe pain. Has 3 main functions: painkiller;
antipyretics; anti-inflammation effect.

Amethocaine 0.5% eye drops single-use vial 1ml or similar substance

Ibuprofen coated tablet 400 mg
Lignocaine 1% (without adrenaline) Ampoule 5ml
Morphine (injectable) ampoule 1 ml = 10mg
Morphine (oral) liquid 1mg/ml 100ml bottle
Naloxone Ampoule 1 ml (=0.4mg) – opioid antagonist ( in case of overdose with
opioids)
Paracetamol Tablets 500mg
Tramadol tablets 50 mg

3. Antiallergic medication
• Asthma attack / Anaphylaxis:
o Adrenaline 1:1000 Ampoule 1ml = 1 mg
o Salbutamol aerosol inhaler 0.1mg/dose
o Dexamethasone ampoule 4mg/ml
o Prednisone tablet 25mg or 20mg

• Local and systemic allergic reactions (all antiallergic medications):

Cetirizine tablet 10mg
Dexamethasone ampoule 4mg/ml
Hydrocortisone 1% cream cream (20 -30 gramm)
Oxymetazoline 0.5% (or equivalent) drops or spray

4. Other medications:
• Heart-related diseases
Acetylsalicylic acid 300mg tablet
Adrenaline 1:1000 Ampoule 1ml = 1 mg
Atropine ampoule 1.2mg/ml or 0,5mg/ml amp.
Frusemide Ampoule 4ml = 40mg (diuretics; use to minimize lungs and periferal
oedema due to heart insufficiency etc.)
Isosorbide dinitrate tablet 5mg sublingual
Metoprolol tablet 100mg
Vitamin K Ampoule 1 ml= 10mg (Used in overdose with Warfarin that cause severe
bleeding due to blocked clot formation)

• Antipsychotics, sedatives, antiepileptic drugs

Diazepam tablets 5mg
Haloperidol Ampoule 1 ml= 5mg
Midazolam ampoule 1ml (= 5mg)
 • Infectious diseases prevention and treatment
Aciclovir 400mg tbl.
Artemether Ampoule 1 ml = (80mg)
Artemether + Lumefantrine tablets 20mg + 120mg
Insecticide spray Permethrine, natural pyrethrins or chlorpyriphosmethyl
Insect repellent lotions for skin Vials for personal use DEET 20-35% formulation or Picaridin
or p-menthane-3,8- diol
Mebenadazole tablet 100mg
Miconazole 2% cream
Miconazol vaginal cream
Permethrin 1% lotion 250 ml
Permethrin 5% Lotion, vial of 50-100 g
Tetanus Immunoglobulin ampoule. (keep at 2-8°C)
Tetanus toxoid vaccination ampoule (keep at 2-8°C)
Zidovudine plus Lamivudine tablet, 300mg+150mg

• Gastrointestinal disorders treatment

Charcoal, activated 50g in 300 ml purified water
Docusate with Senna (or equivalent) tablet 50mg +8mg
Loperamide tablet 2mg
Omeprazole tablets 20mg
Ondansetron tablet 4mg
Oral rehydration salts sachets of powder for reconstitution
Petroleum jelly 50to 100 g (vaseline)*

II. Hypothermia
Accidental hypothermia is an involuntary drop in core temperature below 35°C (<95°F) and can
often be associated with significant morbidity and mortality. Heat is lost from a warm body by
conduction, convection, evaporation, and
radiation. Core temperature may
continue to drop after a patient is
removed from the cold environment, a
process often referred to as afterdrop.
The amount of continued core cooling
will depend on the stage of hypothermia,
the degree of thermoregulatory
dysfunction, the ongoing cold stress
(often significant in the prehospital care
environment), and the physics of heat
transfer (heat from the relatively warmer core will be transferred to the cooler periphery by direct
conduction or by convection from blood flow).
The body attempts to preserve normothermia through mechanisms such as increased metabolic
rate, peripheral vasoconstriction, increased preshivering muscle tone, or shivering. As the core
temperature drops below approximately 35°C, progressive impairment occurs, affecting all
of the body’s organ systems.
Cardiovascular responses to cold include profound peripheral vasoconstriction and an
initial increase in heart rate and blood pressure, usually followed by progressive
bradycardia, hypotension,
and myocardial irritability.
Below approximately 32°C,
the risk of cardiac arrest
increases as malignant
cardiac dysrhythmias become
more common, particularly
below 28°C.
MILD HYPOTHERMIA
(STAGE I)
Otherwise healthy stage I
patients (conscious, shivering, core temperature ≥32°C) can often be rewarmed locally using a
warm environment, provision of dry clothes, warm sweet drinks, and active movement.
MODERATE HYPOTHERMIA (STAGE II)
Stage II patients (impaired
consciousness, may or may
not be shivering, core
temperature ∼28°C to
32°C) require careful
handling, prevention of
further heat loss, active
external and minimally
invasive rewarming (warm
environment; forced air,
electrical, or chemical
warming blankets; warm
parenteral fluids), cardiac
monitoring, and core
temperature monitoring.
SEVERE
HYPOTHERMIA (STAGE III)
Stage III (unconscious, vital signs present, core temperature <∼28°C) patients require the same
treatment as stage II patients and may require intubation for airway protection.
III. Hyperthermia
Heat is generated by cellular metabolism and the mechanical work of skeletal muscle. Heat
accumulates from radiation from the sun and contact with hot objects. Heat is absorbed when the
ambient temperature rises above body temperature. As core temperature rises, the autonomic
nervous system is stimulated to promote sweating and cutaneous vasodilatation. Evaporation is
the principal mechanism of heat loss in a hot environment, but this becomes ineffective above a
relative humidity of 75%. When the ambient temperature rises to >35°C (>95°F), the body can
no longer radiate heat to the environment and becomes dependent on evaporation for heat
transfer. As humidity increases, the potential for evaporative heat loss decreases. The

combination of high temperature and high humidity essentially blocks the two main physiologic
mechanisms that the body uses to dissipate heat. Elevations of temperature are accompanied by
an increase in oxygen consumption and metabolic rate, resulting in hyperpnea and tachycardia.
The physiologic response to heat stress consists of four primary mechanisms: dilatation of
blood vessels, particularly in the skin; increased sweat production; decreased heat production;
and behavioral heat control.
Heat exhaustion and heat stroke occur when the body’s thermoregulatory responses are impaired
or overwhelmed and are no longer capable of maintaining homeostasis. Excessive heat is directly
toxic to cells, causes an acute-phase reaction with release of inflammatory cytokines, and
damages vascular endothelium. Escalating cellular temperature results in denaturation of
proteins, interruption of cellular processes, and cell death. Temperatures of >41.6°C (>106.9°F)
can produce cellular injury in hours. As temperature rises, cellular damage occurs more quickly
and extensively. Temperatures >49°C (>120.2°F) typically result in immediate cell death and
tissue necrosis.
Heat stress is treated with volume and electrolyte replacement and rest.
• Remove the patient from the hot environment immediately, and perform standard
resuscitation measures.
• Check point-of-care glucose if there is altered mental status.
• Start cooling by removing clothing and implementing one of the following methods:
 o spray the patient with water and provide airflow over the patient (ideal method
but not always practical during transportation);
o place wet towels or sheets over the patient’s body;
o place ice on the patient.
• Administer a bolus of normal saline (1 to 2 L) if hypotension is present.

IV. Trench foot

The pathophysiology of trench foot is
multifactorial, but involves direct injury to
soft tissue and peripheral nerves sustained
from prolonged cooling, accelerated by wet
conditions.
Early symptoms progress from subjective
tingling to numbness of the affected tissues.
On initial examination, the foot may appear
pale, mottled, anesthetic, pulseless, and
immobile, with no immediate change after
rewarming.
A hyperemic phase begins within hours after rewarming and is associated with severe burning
pain and reappearance of proximal sensation. As perfusion returns to the foot over 2 to 3 days,
edema and bullae may form. Anesthesia frequently persists for weeks and may be permanent.
In more severe cases, tissue sloughing and gangrene may
develop. Hyperhidrosis and cold sensitivity are common late
features and may persist for months to years. Severe cases may be
associated with prolonged convalescence and permanent
disability.
Treatment is supportive. Feet should be kept clean and warm
and be dryly bandaged, elevated, and closely monitored for early
signs of infection.
Prophylaxis for trench foot includes keeping warm, ensuring
good boot fit, changing out of wet socks several times a day,
never sleeping in wet socks and boots, and, once early symptoms
are identified, maximizing efforts to warm, dry, and elevate the
feet.

V. Sea sickness
Motion sickness is a syndrome that occurs in response to real or perceived motion, which can
include gastrointestinal, central nervous system, and autonomic symptoms.
Motion sickness is considered a physiologic form of dizziness, since it is not indicative of a
disease process and can be induced in nearly all normal human subjects. There is enormous
variability in susceptibility to motion sickness, as it may be produced with minimal provocation
in some individuals but can be very difficult to elicit in others.
The symptoms of motion sickness were first described by Hippocrates. They frequently occur
during boat travel, and the principal symptom (nausea) is derived from the Greek word for ship
(naus).
CLINICAL PRESENTATION
The syndrome of motion sickness is easily recognized, since it includes stereotypic symptoms in
the setting of passive motion or in the setting of visual perception of motion without actual
movement.

The most characteristic symptom of motion sickness is nausea, a feeling of warmth and malaise.
Nausea can progress to vomiting, which is occasionally severe. Some patients may experience
headache with their motion sickness.
Other symptoms may include nonvertiginous dizziness, belching, increased salivation,
diaphoresis, and a general feeling of malaise. Hyperventilation is a common associated feature
and can induce dyspnea, paresthesias, and feelings of impending doom.
Physical signs usually cannot be detected, although pallor may be present.
Symptoms typically subside after 36 to 72 hours of continuous exposure, but they can recur upon
returning to the pre-exposure environment (eg, returning to land after a sea voyage).
APPROACH TO MANAGEMENT
• Looking at the horizon or a distant, stationary object.
• Avoidance of reading or looking at a screen while in a moving environment, as this can
increase conflict between vestibular and visual cues.
• Selecting seats where motion is the least. In a boat, lower deck and midship cabins are
recommended.
• Radio consultation for preferable medications for administration in case of sea sickness
VI. Intoxication
Exposures occur most commonly by ingestion; other routes include inhalation, insufflation,
cutaneous and mucous membrane exposure, and injection. Some exposures have minimal risk.
The criteria used to determine whether the exposure is nontoxic are as follows:
1. an unintentional exposure to a clearly identified single substance,
2. an estimate of the dose is known, and
3. a recognized information source (e.g., a poison control center) confirms the substance as
nontoxic in the reported dose.
Asymptomatic patients with nontoxic exposures may be discharged after a short period of
observation, providing they have access to further consultation and a safe discharge destination.
Stabilization of airway, breathing, and circulation represents initial priorities.
Compromised airway patency or reduced respiratory drive may lead to inadequate ventilation;
provision of a mechanical airway and assisted ventilation is vital in these circumstances. IV
crystalloid bolus (10 to 20 mL/kg) is first-line treatment of hypotension. Vital signs stabilization
allows further assessment of blood glucose concentration, temperature, and conscious state.
Although the proper use of antidotes is important, only a few are indicated before
cardiopulmonary stabilization (e.g., naloxone for opiate toxicity, cyanide antidotes for cyanide
toxicity, and atropine for organophosphate poisoning).
OCULAR DECONTAMINATION
Eye exposures may require local
anesthetic (e.g., 0.5% tetracaine)
instillation and lid retractors to
facilitate copious irrigation with
crystalloid solution. Alkalis produce
greater injury than acids due to deep
tissue penetration via liquefaction so
that prolonged irrigation (1 to 2
hours) may be required. Ten minutes
after irrigation (allowing equilibration of crystalloid and conjunctival sac pH), conjunctival sac
pH is tested. Irrigation continues until pH is between 7.2 and 7.4. Ophthalmologic consultation is
indicated for all ocular alkali injuries.
GI DECONTAMINATION
!!!! DO NOT CAUSE VOMITING !!!!
1) Single-Dose Activated Charcoal
Super-heating carbonaceous material produces activated charcoal, a highly porous substance,
which is suspended in solution and given PO as a slurry. Toxins within the GI lumen are
adsorbed onto the activated charcoal and carried through the GI tract, limiting absorption.
Activated charcoal does not effectively adsorb metals, corrosives, and alcohols. The decision
to give activated charcoal requires individual patient risk assessment and is not routinely
indicated following all oral exposures.
2) Whole-Bowel Irrigation
Polyethylene glycol is an osmotically balanced electrolyte solution. Administration in large
quantities mechanically forces substances through the GI tract, limiting toxin
absorption.Polyethylene glycol can be administered orally to cooperative, awake patients,
but consider formal airway control if consciousness is likely to deteriorate. Minimize risk of
pulmonary aspiration during whole-bowel irrigation by patient positioning (head up 30 degrees),
ensuring bowel sounds are present during fluid administration, 1:1 nursing with suctioning of the
oral cavity during infusion, and utilization of cuffed endotracheal tubes.
SKIN DECONTAMINATION
Decontamination is required for toxic exposures affecting large dermal areas. Healthcare
providers wearing personal protective equipment (if indicated) or observing universal
precautions (gown, gloves, eye protection) should assist with undressing and washing the patient
using copious amounts of water (min.10 minutes). Contaminated clothing is collected, bagged,
and properly disposed. Decontamination ideally occurs in a separate area to minimize cross-
contamination.
AIRWAY DECONTAMINATION
Main symptoms:
1) headaches
2) pale skin
3) hyperventilation
4) caugh; difficulty breathing
Casuality needs to be transported in the area with
a fresh air; additive high-concentration oxygen
mask preferably is used (10 L/min – 15 L/min).
In case of loss of consciousness ABC algorythm
must be used.
VII. Dental problems
ANATOMY OF THE TEETH
A tooth consists largely of
dentin, which surrounds the
pulp, the tooth’s neurovascular
supply Dentin is a
homogeneous material
produced by pulpal
odontoblasts throughout life.
Dentin is deposited as a system
of microtubules filled with
odontoblastic processes and
extracellular fluid. The crown,
or the visible portion of tooth,
consists of a thick enamel layer
overlying the dentin. Enamel,
the hardest substance in the
human body, consists largely
of hydroxyapatite and is
produced by ameloblasts
before eruption of the tooth
into the mouth. The root
portion of the tooth extends
into the alveolar bone and is
covered with a thin layer of
cementum.

DENTAL CARIES AND PULPITIS

Dental caries is the loss of integrity of the tooth enamel from hydroxyapatite dissolution by
prolonged exposure to the acidic metabolic by-products of plaque bacteria.
• A local anesthetic block greatly reduces pain and should be considered for short-term
pain management.
• NSAIDs with or without acetaminophen as an adjunct are recommended by the American
Dental Association over narcotics for managing dental pain because NSAIDs offer the
most favorable balance between pain reduction and potential harms.
• The definitive treatment for irreversible pulpitis and pulpal necrosis is root canal therapy
or dental extraction.
PERIRADICULAR PERIODONTITIS
Acute periradicular periodontitis is the extension of pulp disease, inflammation, or necrosis into
the tissues surrounding the root and apex of the tooth (deepest portion of the tooth socket).
Occasionally it can be due to occlusal trauma.
Treat dental abscesses or other periapical lesions with appropriate antibiotics after tele-
radio medical consultation.. NSAIDs with or without supplemental acetaminophen are preferred
over opiates by the American Dental Association for pain relief.6 Refer to a dentist for definitive
treatment.

GINGIVAL AND PERIODONTAL ABSCESS

A gingival abscess is an acutely painful swelling confined to the margin of the gingiva or
interdental papilla. It usually rapidly enlarges over 24 to 48 hours, and purulent exudate can
frequently be expressed from the orifice. The most common etiology is the entrapment of foreign
matter such as a popcorn kernel, piece of meat, toothbrush bristle, or piece of food in the gingiva.
Treatment includes: identifying and removing the embedded foreign body and irrigating with
normal saline. Continued home irrigation is beneficial, and symptoms resolve quickly.

VIII. Disease prevention and hygiene

Portals for infectious disease entry are percutaneous, mucous membrane (oral, ocular, nasal,
vaginal, or rectal), respiratory, and dermal. The risk of infection depends on:
• the route (portal) of exposure,
• the concentration (number of organisms) of the pathogen in the infectious material,
• the infectious characteristics (virility) of the pathogen,
• the volume (dose) of infectious material, and
• the immunocompetence (susceptibility) of the exposed individual.

1) Percutaneous exposures pose the highest risk of transmission for bloodborne disease. Needle
sticks and lacerations by sharp objects account for most percutaneous injuries.
2) Mucous membrane exposures result from splatters, splashes, and sprays of blood and body
fluids. Tasks associated with risk of mucous membrane exposure include wound management
(hemorrhage control, exploration, irrigation, debridement), airway suctioning, nasogastric or
orogastric tube placement, intubation, and specimen handling.
3) Respiratory exposures occur through inhalation of airborne or droplet particulate materials.
Exposure risk grows when an individual is confined with an expectorating, coughing, or
sneezing patient for prolonged periods or in a poorly ventilated environment.
4) Dermal exposure involves skin contact with patients, environmental surfaces, or objects
contaminated with infectious material. The risk of infection increases if the contact involves a
large surface area or nonintact skin (abraded, chapped, or excoriated). Drug-resistant organisms
(e.g., methicillin-resistant Staphylococcus aureus, vancomycin-resistant enterococci) and
parasites of the integument (e.g., scabies, lice) are transmitted by dermal exposure.
Hand hygiene with soap and water or alcohol-based hand sanitizer is one of the most
important ways to prevent the spread of infection.
The World Health Organization recommends in case of medical assistance to clean hands:
• before touching a patient,
• before a clean/aseptic procedure,
• after body fluid exposure/risk,
 • after touching a patient
• after touching a patient’s surroundings.
Using sterile or nonsterile gloves does not eliminate the need for hand hygiene; hand
hygiene should be performed both before and after gloves are used.
FOOD AND WATERBORNE ILLNESSES
Foodborne illness occurs after consumption of a food contaminated with bacteria, viruses, or
protozoans. Outbreaks from contaminated food are often widespread due to advances in modern
food logistics.
Viruses are the most common cause of foodborne disease, with the norovirus causing more
than half all cases and 26% of all admissions.
Other viral sources of infection include rotavirus, astrovirus, and enteric adenovirus.
Although less frequent, bacterial causes tend to be more severe, with nontyphoidal Salmonella
and Listeria most often resulting in fatality. Other common bacterial causes of foodborne illness
include: Clostridium perfringens, Campylobacter spp., Toxoplasma gondii, Shigella,
Staphylococcus aureus, and Shiga toxin–producing Escherichia coli (STEC).
There are three basic mechanisms by which microbes cause illness:
• produce toxins causing illness (S. aureus, Bacillus cereus, and Clostridium botulinum)
These toxins are present in the food before ingestion and result in the rapid onset (1 to 6 hours)
of symptoms trigger the accompanying nausea and vomiting.
• Toxin production after ingestion, which interacts with intestinal epithelium ( Vibrio,
Shigella, and STEC)
These cause diarrhea (sometimes bloody) and lower abdominal cramping, with onset at
approximately 24 hours after exposure. Some toxins produced by Vibrio and enterotoxigenic E.
coli produces a large fluid shift into the intestinal lumen, which overwhelms the absorptive
capacity of the colon causing watery diarrhea.
• Direct invasion of the intestinal epithelium ( enteric viruses, notably Salmonella,
enteroinvasive E. coli, and Campylobacter)
This causes diarrhea due to transient malabsorption that is frequently bloody and accompanied
by fever. Illness requires ingestion of just a few pathogens to cause disease. The upper and lower
GI symptoms from invasive organisms last from 24 hours to weeks.
TREATMENT
Most episodes of acute gastroenteritis require adequate hydration and supportive care.
The World Health Organization recommends initial oral hydration with a glucose-containing
fluid (i.e., Pedialyte® or equivalent).
Reserve parenteral rehydration for patients with severe dehydration or with continued vomiting
and inability to tolerate oral fluids. Antiemetics may reduce vomiting, ED length of stay, and
need for admission.
Antimotility medications, such as loperamide, may decrease illness duration for mild to
moderate nonbloody diarrhea in adults without fever.
RADIO-MEDICAL ADVICE !
MALARIA
The classic clinical triad for all
species of malaria is:
• Fever
• Splenomegaly
• Thrombocytopenia
Fever is typically irregular for the
first week and later may be
periodic. Patients usually have
continuous symptoms initially
followed by episodic pyrexia every
2 to 3 days, depending on the
infecting species. Because associated
symptoms such as headache, cough,
and GI problems mimic other
conditions, malaria should be a
consideration in all febrile travelers.
If a patient has the appropriate
travel history and altered mental
status, suspect cerebral malaria
and initiate treatment promptly.
Diagnosis is based on clinical presentation
• Patients with fever >38.5°C (101.4°F) of unclear origin
• recent or past travel to an endemic area
• Yellow skin tone
• Headaches, dizziness, difficulty breathing, low O2 saturation;
• Hypotension and rapid pulse

DENGUE FEVER
The World Health Organization reports a 30-fold increase in incidence of dengue in the past 30
years, becoming a leading cause of morbidity and mortality in the tropics. Suspect dengue fever
among travelers with fever developing within 2 weeks of travel. Dengue may be contracted
more than once, and subsequent infections may be progressively more severe.
Symptoms:
Dengue is transmitted by the
day-biting Aedes aegypti
mosquito. Dengue fever
presents after a typically short
incubation period of 4 to 7
days with sudden high fever,
headache, nausea, vomiting,
severe myalgias (hence the
term “break bone fever”), and
rash usually lasting several
days. Facial flushing,
conjunctival injection
(although uncommon), and
retro-orbital pain can occur.
After defervescence, a fine,
pale, morbilliform rash
develops on the trunk and
spreads to the extremities and
face. Dengue may be confused
with influenza, measles, or
rubella. West Nile fever can
also present similarly, but also
causes lymphadenopathy
(enlarged lymphnodes), which
is usually absent in dengue.
Diagnosis of dengue is based on clinical findings.
Treatment:
In uncomplicated dengue fever, treatment is supportive and consists of fluids and analgesics.
Only acetaminophen is recommended for managing pain and fever because aspirin and
other NSAIDs are contraindicated due to anticoagulant properties.

YELLOW FEVER
Yellow fever, an acute zoonotic flavivirus, has a jungle monkey reservoir present in the tropics
of South America and Africa, where vaccination is mandatory. Outbreaks are common near
tourist areas and may occur among nonimmunized adventure travelers who travel to endemic
areas. With the increase in global travel and because the day-biting mosquito vector A. aegypti
(which also transmits dengue) is endemic in a wide global distribution, including North and
Central America, the Caribbean, as well as parts of Asia, yellow fever outbreaks can appear
outside of traditionally endemic areas, as evidenced by a recent outbreak in Brazil.
Yellow fever ranges in severity from an undifferentiated self-limited flulike illness to a
hemorrhagic fever that is fatal in 20% to 50% of patients who develop severe disease (15% of
infected persons).
Symptoms:
After an incubation of 3 to 6 days, patients develop fever, headache, myalgias, conjunctival
injection, abdominal pain, prostration, facial flushing, and relative bradycardia.
In most cases, patients recover, but in others moderate symptoms occurs:
fever remission lasts a few hours to several days, followed by renewed high fever, jaundice,
vomiting, shock, multiorgan failure, and bleeding diathesis. The classic presentation is a triad
of jaundice, black emesis, and albuminuria.
Severe symptoms: Confusion, seizures, and coma are common in the late stages of the illness,
and death can occur within 7 to 10 days after onset.

Treatment is supportive, with fluid replacement and management of hematologic complications.

EBOLA AND MARBURG VIRUSES

Symptoms begin 2 to 21 days after exposure with fever, myalgia, malaise, diarrhea, abdominal
pain, and vomiting, and progress to hemorrhage, shock, and end-organ failure. Mortality is
high, but those who recover have an antibody response that lasts about 10 years.
Treatment is supportive with no proven effective antiviral therapy.
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1) https://www-uptodate-com.db.rsu.lv/contents/motion-
sickness?search=sea%20sickness&source=search_result&selectedTitle=1~77&usage_type=
default&display_rank=1
2) https://accessmedicine-mhmedical-
com.db.rsu.lv/content.aspx?bookid=2353&sectionid=220744030#1174959838
3) https://www.agcorporation.ae/images/eyewash-banner.jpg
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com.db.rsu.lv/content.aspx?bookid=2353&sectionid=221180004#1166813845
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com.db.rsu.lv/content.aspx?bookid=2353&sectionid=220746470
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com.db.rsu.lv/content.aspx?bookid=2353&sectionid=220293375#1166598064
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