4 PERINATAL ASPHYXIA

Definition[1]
Interference in gas exchange between the organ systems of the
mother and fetus resulting in impairment of tissue perfusion and
oxygenation to vital organs of the fetus such that arterial carbon
dioxide partial pressure rises, and arterial oxygen partial pressure
and pH fall. When the arterial oxygen partial pressure is very low,
anaerobic metabolism occurs producing large quantities of
metabolic acids.
Epidemiology

About 40% of all under five deaths occurred in the neonatal

period in 2008; in the same period asphyxia was the cause of
9% of all under five deaths[4]
Incidence[5]

Resource-rich countries: 1/1000 live births

Resource-poor countries: 5 10/1000 live births

Etiopathogenesis[1]
INTRAPARTUM ASPHYXIA

Aerobic
metabolism

Hypoxia

Etiology 5 causes during labor and delivery:

1. Interruption of umbilical blood flow (e.g. cord compression)
2. Failure of gas exchange across the placenta (e.g. placental
abruption)
3. Inadequate perfusion of the maternal side of the placenta
(e.g. severe maternal hypotension)
4. A compromised fetus who cannot further tolerate the transient,
intermittent hypoxia of normal labor (e.g. anemic, growthretarded)
5. Failure to inflate the lungs and complete the change in
ventilation and lung perfusion that must occur at birth
Clinical manifestations Criteria for diagnosis:
1. Fetal acidosis (pH < 7.0 or Base excess > 12 mmo/L)
2. APGAR score of 0 3 at 5 minutes
3. Seizure
4. Multi-system organ dysfunction
APGAR SCORE[3]

Objective measurement of the newborns condition and

response to resuscitation normally assigned at 1 minute and
again at 5 minutes

NOT used alone to determine the NEED for resuscitation or to

guide the resuscitation efforts

Resuscitation must NOT be delayed for the purpose of

tabulating APGAR score

Hypercapnea

Decreased pH

Redistribution of blood flow

Increased:
Heart
Brain
Adrenals

Oxygen debt to the brain

Cytotoxic
edema

Vasogenic
edema

Brain swelling

Blue, pale

Heart rate
Respiration
Reflex
irritability

Increased
Lactate

Altered brain H20

distribution

SCORE 0

Color
Muscle tone

Anaerobic
metabolism

Decreased:
Lungs
Kidneys
GI tract

PARAMETER

Altered brain
cerebral blood flow
Multifocal tissue
ischemia
Generalization

Cytotoxic edema all the cellular elements (neurons, glia, and

endothelial cells) imbibe fluid and swell, with a corresponding
reduction in ECF space
Vasogenic edema increased capillary permeability leads to
escape of plasma infiltrate into the intracellular space through
incompetent tight junctions

SCORE 1
Body pink, extremities
blue

None,
limp
0
Absent

< 100
Slow, irregular

None

Some grimace

Slight flexion

SCORE 2
Totally pink
Active, good
flexion
> 100
Strong, regular
Good grimace,
crying

Interpretation of 1 minute APGAR score:

> 7: requires minimal resuscitation other than drying and

stimulation

4 to 6: mild to moderate asphyxia, more vigorous

resuscitation may be required (supplemental oxygen,
vigorous stimulation)

< 3: moderate to severe asphyxia, aggressive

resuscitation should be started immediately

Management

1.

American Academy of Pediatrics and American Heart Association

Algorithm for Neonatal Resuscitation[3,7]
Birth

Term gestation?
Clear amniotic fluid?
Breathing or crying?
Good muscle tone?

Yes

Routine care:
Provide warmth
Clear airway
Dry
Assess color

30 s

No
Provide warmth1
Position; clear airway (as
necessary); clear mouth
and nose of secretions2
Dry, stimulate3, reposition

For meconium stained

depressed infants4
Do direct mouth
and tracheal
suctioning

2.

3.

Evaluate respirations,
heart rate, and color
Apneic or HR < 100

Breathing, HR > 100

but cyanotic

4.

30 s

Give
supplemental
oxygen5
Persistently cyanotic
Provide positive-pressure ventilation6
5.
HR < 60

HR < 60

30 s

Provide positive-pressure ventilation

Administer chest compressions7
HR < 60

HR < 60
Administer epinephrine8

Endotracheal intubation9 may become necessary if

positive-pressure delivery by mask is not helpful

Recheck effectiveness:
Ventilation
Chest compressions
Endotracheal intubation
Epinephrine dlievery
Consider possibility of
HYPOVOLEMIA10

HR <60,
Persistent
cyanosis,
Failure to
ventilate

Consider:
Airway malformations
Lung problems:

Pneumothorax11

Diaphragmatic
hernia12
Congenital heart
disease

Consider discontinuing resuscitation

6.

Temperature Control

Newborns are at risk for hypothermia following delivery

because of their,

Large surface area to mass ratio

Evaporative heat loss

Hypothermia can lead to:

Hypoglycemia

Increased oxygen consumption

Respiratory
depression
and
acidosis
(if severe)

Dry infant with warm towels and place infant under

radiant heat source

Very low birth weight infants (< 1,500 g) are especially

prone to hypothermia and may need to be placed under
plastic wrapping to avoid evaporative loss

Avoid hyperthermia as this may worsen ischemic brain

injury
Positioning

Place head into a sniffing position

This position aligns the posterior pharynx, larynx, and

trachea, and allows for unimpeded air entry

NOTE: Excessive extension or flexion of the neck may

result in airway occlusion

Perform oral and nasal suctioning with a bulb syringe or

suction catheter
Stimulation

For vigorous newborns, drying and suctioning of the

mouth are usually adequate to increase heart rate and
respiratory effort

If respiration is not adequate, flick the soles of the feet or

rub the infants trunk

If no response is observed to tactile stimulation, initiate

Positive Pressure Breaths
Meconium

VIGOROUS newborns do NOT require endotracheal

suctioning of meconium

Indication for endotracheal suctioning of meconium:

DEPRESSED newborns

Absent or depressed respirations

Heart rate < 100 bpm

Poor muscle tone

Reassess newborns clinical status after every attempt

Institute PPV if infant becomes severely depressed or

bradycardic
Oxygen

ALL infant with central cyanosis (mouth and tongue)

should be provided free-flow oxygen even if they present
only with mild respiratory distress

Acrocyanosis (hands and feet) represents peripheral

vasoconstriction and is NOT an indication for oxygen

Administer 5 L/min 100% via face mask or flow inflating

bag mask held over the infants nose
Ventilation

Indications:

Infant remains apneic or gasping

Heart rate < 100 bpm after 30 seconds of initial

resuscitation

Central cyanosis DESPITE supplemental oxygen

Technique

Possible routes:
(1) Cushioned mask with a flow inflating bag
(2) T-piece connector

Use 100% oxygen, or room temperature PPV (if

unavailable)

Peak pressure set up to 40 cm H2O due to stiff fluid

filled lungs of newborns, lower once fluid begins to
express from the lungs to avoid iatrogenic
pneumothorax

Bag-mask ventilation at 40 60 breaths per minute is

continued for 30 seconds, then infant is reassessed

Discontinue once,

Heart rate is > 100 bpm

Infant is breathing spontaneously

Improvement in color and tone

Continue if Heart rate is < 100 bpm

Initiate chest compressions if Heart rate remains < 60 bpm

and perform intubation
7. Chest compressions

Indication: Heart rate is < 60 bpm despite 30 seconds of

effective PPV

Guidelines:

Deliver over lower 1/3 of sternum, depth of 1/3 the

AP diameter of the chest cavity

3:1 compression to ventilation ratio every 2 seconds

(90 compressions and 30 ventilations/minute)

Every 30 seconds re-evaluate respiratory effort, color,

pulse, muscle tone

Two finger technique

Two fingers (middle and ring) are used to deliver

compression while the other hand supports the back

Two thumb circling hand technique

More effective: higher peak systolic and coronary

perfusion pressure

Two thumbs deliver the compression with providers

hands encircling infant and supporting the back

Discontinue if Heart rate is > 60 bpm

8. Epinephrine

Indications:

Asystole

Bradycardia (Heart rate < 60 seconds after 30

seconds of effective PPV with 100% oxygen and
chest compressions)

Recommended IV dose: 0.1 to 0.3 ml/kg (0.01 to 0.03

mg/kg) per dose of 1:10000 solution

Higher doses are NOT recommended from studies

showing:
(1) Exaggerated hypertension
(2) Decreased myocardial function
(3) Worse neurologic function (dose 0.1 mg/kg)

Recommended ET tube dose while IV access is being

obtained: 0.3 to 1 ml/kg

Can be repeated every 3 to 5 minutes, re-evaluate

patient carefully between doses
9. Endotracheal intubation

Indications:

Poor response to/inability to provide adequate PPV

Need for endotracheal suctioning or chest

compressions

Extreme prematurity

Suspected diaphragmatic hernia

Successful intubation is evidenced by bilateral chest rise

and improvement of heart rate, color, and muscle tone

IF ET tube is advanced too far, maintstem bronchus

intubation occurs and breath sounds are diminished over
half of the chest, withdraw tube slowly until equal bilateral
breath sounds are auscultated

Formula for depth of intubation:

Depth in cm = 6 + infants weight (in kg)

Monitor
oxygen
saturation
and
evidence
of
pneumothorax
10. HYPOVOLEMIA

Clinical manifestations:

Pallor

Weak pulses

Delayed capillary refill

Persistent bradycardia

Failure to respond to well-administered resuscitation

Given in aliquots of 10 ml/kg over 5 to 10 minutes with

Normal Saline Solution

Follow with packed RBCs if there is large volume blood

loss or poor response to crystalloid

11. PNEUMOTHORAX

Can rapidly lead to Tension Pneumothorax and

potentially lethal cardiorespiratory compromise

Risk factors:

Prematurity

Meconium aspiration syndrome

Clinical manifestations:

Tachypnea

Retractions

Grunting

Tachycardia

*Bradycardia with symptoms of shock in Tension

Pneumothorax

If significant respiratory distress is present perform needle

decompression using a 20 gauge needle placed into the
affected lung either in:

4th ICS AAL

2nd ICS MCL

12. DIAPHRAGMATIC HERNIA

Defect in the diaphragm, usually on the left side, gives rise

to displacement of the lung by abdominal contents
entering the chest cavity

Clinical manifestations:

Respiratory distress

Cyanosis

Scaphoid abdomen

Place gastric tube to decompress stomach, administer

oxygen

Intubate and start PPV

AVOID bag-mask ventilation as this will lead to

gastric distention and further respiratory compromise
References
1.
2.
3.
4.
5.
6.

7.

Perinatal Asphyxia by Dr. Emilio A. Hernandez from the Handbook of

Medical and Surgical Emergencies, 6th ed, published by Elsevier 2007
USMLE Roadmap: Biochemistry by Richard G. Macdonald and William
G. Chaney, published by Lange 2007
Pediatric Emergency Medicine, 3rd edition, Gary R. Strange et al
Guidelines on Basic Newborn Resuscitation by the World Health
Organization 2012
Perinatal Asphyxia by William McGuire from the British Medical Journal
published on March 2007
Pathophysiology of perinatal asphyxia: can we predict and improve
individual outcomes? By Paola Morales, et al from the Official Journal
of the European Association for Predictive, Preventive, and
Personalized Medicine published on June 2011
Textbook of Neonatal Resuscitation, 5th edition, American Academy of
Pediatrics and American Heart Association

8 DIARRHEAL DISEASES AND DEHYDRATION

Definitions

Diarrhea passage of 3 or more liquid stools in a 24 hour

period, with the more important feature being the consistency
rather than the number of stools. Best described as excessive
loss of fluid and electrolyte in the stool.

Acute lasting for a few hours or days

Chronic (persistent) lasting for 2 weeks or longer

Dysentery small-volume, frequent bloody stools with mucus,

tenesmus, and urgency

Dehydration

Loss of fluid without loss of supporting tissues

Contraction of extracellular volume in relation to cell mass

Most common disturbance of water balance in pediatrics

May result from:

1. External loss of water and salt
2. External loss of salt without water deficit
3. External loss of water alone
Epidemiology (1993 Statistics from the Health Intelligence Service)

Leading cause of morbidity and 9th leading cause of mortality

for all ages

4th leading cause of death among infants in the Philippines

Mortality due to delayed replacement of fluid and electrolyte

losses, and starvation leading to acute dehydration and
malnutrition
Common Etiologic Agents
VIRUSES
Rotavirus
Norwalk
agent
Adenovirus
Calicovirus
Coronavirus
Astrovirus

BACTERIA
Escherichia coli
(Enterotoxigenic, Enteropathogenic,
Enteroinvasive, Enterohemorrhagic,
Enteroadherent)
Vibriocholerae
Shigella
Campylobacter jejuni
Staphyloccocus aureus
Clostridium difficile
Clostridium perfringens
Yersinia enterocolitica
Vibrio parahaemolytica
Aeromonas hydrophila
Bacillus cereus

PARASITES
Entamoeba histolytica
Giardia lamblia
Strongyloides
Trichuris trichuria
Cryptosporidia

Mechanism
Cause

INCREASED INTESTINAL MOTILITY

Decreased transit time

Stool
Examination
Examples

Loose to normal-appearing stool,

stimulated by gastrocolic reflex
Irritable bowel syndrome,
thyrotoxicosis, postvagotomy
dumping syndrome
Infection may contribute to
increased motility

Effect of
infection
Mechanism
Cause
Stool
Examination
Examples

DECREASED INTESTINAL MOTILITY

Defect in neuromuscular unit(s)
or Stasis due to bacterial
overgrowth
Loose to normal-appearing stool
Pseudo-obstruction, blind loop

Possible bacterial overgrowth

present

MUCOSAL INFLAMMATION
Inflammation, decreased mucosal surface area and/or colonic
reabsorption, increased motility
Blood and increased WBCs in stool
Celiac disease, Salmonella, Shigella, Amebiasis, Yersinia,
Campylobacter, Rotavirus, enteritis

Evaluation
ASSESS HYDRATION STATUS
General
condition
Eyes
Tears
Mouth and
tongue

GROUP A

GROUP B

Well, alert

Restless, irritable

Normal
Present

Sunken
Absent

Moist

Dry

Very dry

Thirst

Not thirsty, drinks

normally

Thirsty, drinks eagerly

Skin pinch

Goes back quickly

< 2 seconds

Goes back slowly

> 2 seconds

Status

NO DEHYDRATION

SOME DEHYDRATION

PLAN A

PLAN B

Drinks poorly or not

able to drink
Goes back very
slowly
> 3 seconds
SEVERE DEHYDRATION

PLAN C

Persistent
vomiting or
refuses to
drink

Patient improves

GROUP C
Lethargic,
unconscious, floppy
Very sunken and dry
Absent

If improved,
revert to Plan
A or Plan B

Patient worsens

Common Differential Diagnoses

INFANT
Acute

Chronic

Gastroenteritis
Systemic infection
Antibiotic associated
Postinfectious
secondary lactase
deficiency
Cows milk/soy protein
intolerance
Chronic nonspecific
diarrhea
Celiac disease
Cystic fibrosis
AIDS enteropathy

CHILD
Gastroenteritis
Food poisoning
Systemic infection
Antibiotic associated
Postinfectious
secondary lactase
deficiency
Irritable bowel syndrome
Celiac disease
Lactose intolerance
Giardiasis
Inflammatory bowel
disease
AIDS enteropathy

ADOLESCENT
Gastroenteritis
Food poisoning
Antibiotic associated
Irritable bowel
syndrome
Inflammatory bowel
disease
Lactose intolerance
Giardiasis
Laxative abuse
(Anorexia nervosa)

Pathophysiology
Mechanism
Cause

Stool
Examination
Examples

Effect of
fasting

SECRETORY
Secretagogue (e.g. Cholera toxin)
binds to receptor on the surface of the
epithelium of the bowel to stimulate
intracellular accumulation of cAMP or
cGMP leading to excessive secretion
with decreased absorption
Watery, normal osmolality

Cholera, Toxigenic E. coli, carcinoid

syndrome, VIP, neuroblastoma,
congenital chloride diarrhea,
Clostridium difficile cryptosporidiosis
(AIDS)
Persists during fasting

OSMOTIC
Ingestion of poorly absorbed
solute which is fermented in
the colon producing Short
Chain Fatty Acids, increasing
osmotic solute load
Watery, acidic, (+) reducing
substances, increased
osmolality
Lactase deficiency, glucosegalactose malabsorption,
lactulose, laxative abuse

NGT

Management
PLAN A: TREAT DIARRHEA AT HOME
Indications:
1. Children with no dehydration
2. Improved status after Plan B or C
3. Children that cannot be returned to the health worker if
diarrhea gets worse
Goals:
1. Treat childs current episode of diarrhea at home
2. Give early treatment for future episodes of diarrhea
Three rules for treating diarrhea at home:
1. Give the child more fluids than usual to prevent dehydration

Use a recommended fluid such as ORS. If this is not

possible, give plain water.

Give as much of these fluids as the child will take.

Continue giving these fluids until the diarrhea stops

Instructions: Dissolve 1 packet of ORS solution in 200 ml of

water and give as follows,
AGE
< 24 months
2 10 years
> 10 years

Stops with fasting

AMOUNT AFTER EACH LOOSE STOOL

50 100 mL
100 200 mL
As much as wanted

MAINTENANCEA
500 mL/day
1000 mL/day
2000 mL/day

For under 2 years, give teaspoonful every 1 to 2 minutes

For older, give frequent sips from a cup
If child vomits, wait for 10 minutes then give solution more
slowly thereafter
Give ORS packets enough for 2 days of treatment

2.

3.

Give the child plenty of food to prevent under nutrition

Continue to breastfeed frequently

If not breastfed, give usual milk

If < 6 months old and not yet taking solid food, dilute milk
formula with equal amount of water for 2 days

If > 6 months or already taking solid food,

Give cereal or other starchy food mixed with

vegetables, meat, or fish. Add 1 to 2 teaspoonfuls of
vegetable oil to each serving

Give fresh fruit juice or mashed bananas to provide

Potassium

Give freshly prepared food. Cook and mash or grind

food well

Encourage child to eat, offer at least 6 times daily

Give same foods after diarrhea stops, give extra

meal each day for 2 weeks
Take child to health worker if child does not get better in 3
days or develops any of the following:

Many watery stools

Repeated vomiting

Marked thirst

Eating or drinking poorly

Fever

Blood in stool

PLAN B: TREATMENT OF SOME DEHYDRATION

1. Approximate amount of ORS solution to give in the first 4 hours:

If weight is unknown,
Age
Wt
mL

< 4 mon
< 5 kg
200 400

3.

4.

12 23 mon
8 10 kg
600 800

2 4 yrs
11 15.9 kg
800 1200

5 14 yrs
16 29.9 kg
1200 2200

> 15 yrs
> 30 kg
> 2300

If weight is known,

Approximate ORS to be given by:

Weight in kg x 0.75 mL

If the child wants more ORS, give more

Encourage mother to continue breastfeeding

For infants < 6 months who are not breast fed, also give
100 200 ml clean water during this period
Observe the child carefully and help the mother give ORS

For under 2 years, give teaspoonful every 1 to 2 minutes

For older, give frequent sips from a cup

If child vomits, wait for 10 minutes then give solution more

slowly thereafter

If the childs eyelids become puffy, stop ORS and give

plain water or breast milk then give ORS according to
plan A when puffiness is gone
After 4 hours, reassess the child

No signs of dehydration (+) Urine output, child falls

asleep Plan A

Signs of dehydration Repeat Plan B but offer food, milk,

juice as in Plan A

Signs of severe dehydration Plan C

If mother must leave before completing Plan B

Instruct how much ORS to finish in 4-hour treatment

Give ORS packets enough for rehydration and 2 days

2.

1 11 mon
5 7.9 kg
400 600

PLAN C: TREATMENT OF SEVERE DEHYDRATION

Can you give
intravenous (IV)
fluids
immediately?

Yes

No

Is IV treatment
available nearby
(within 30 mins)?
No

Are you trained to

use a nasogastric
tube for
rehydration?
OR
Can the patient
drink?

Yes

Yes

If patient can drink give ORS PO while setting up

Start IVF immediately: 100 mL/kg Ringers Lactate
Solution or NSS as follows,
First give
AGE
Then give 70 mL/kg
30 mL/kg
< 12 mon
1 hour
5 hours
Older
30 mins
2.5 hours
Repeat once if radial pulse is still very weak or not
detectable
Reassess the patient every 1 2 hours. If hydration is
not improving, give IV drip more rapidly
As soon as patient can drink give ORS (5 mL/kg/hr)
usually after 3 4 hours (infants) or 1 2 hours (older)
After 6 hours (infants) or 3 hours (older) re-evaluate
hydration status and treat accordingly

Send patient immediately for IV treatment

If patient can drink provide mother with ORS and
show her how to give it during the trip

Start rehydration by tube/PO with ORS: Give 20

mL/kg/hr for 6 hours (total of 120 mL/kg)
Reassess the patient every 1 2 hours
Repeated vomiting or increasing abdominal
distension Give fluid more slowly
If hydration not improved in 3 hours IVF
After 6 hours, reassess and choose appropriate
treatment plan

No

URGENT: Send the

patient for IVF or
NGT treatment

If possible, observe the patient at least 6 hours after

rehydration to be sure mother can maintain hydration giving
ORS by mouth
If patient is > 2 years old and there is cholera in your area, give
appropriate oral antibiotic when patient is alert

MANAGEMENT OF ASSOCIATED PROBLEMS

1. Blood in the stool

Treat for 5 days with an oral antibiotic recommended for

Shigella
in
your
area:
Trimethoprim
(TMP)
+
Sulfamethoxazole (SMX)

Children: TMP 5 mg/kg + SMX 25 mg/kg BID for 5 days

Adults: TMP 160 mg + SMX 800 mg BID for 5 days

Teach the mother to treat the child as described in Plan A

See the child again after 2 days if:

< 1 years old

Initially dehydrated

There is still blood in the stool

No improvement

If the stools is still bloody after 2 days change oral

antibiotic to alternative recommended for Shigella in your
area,
(1)
Nalidixic Acid

Children: 15 mg/kg QID for 5 days

Adults: 1 g TID for 5 days

(2)
Ampicillin

Children: 25 mg/kg QID

2. Persistent diarrhea (> 14 days)

Refer to the hospital if:

< 6 months old

Dehydration is present (treat first then refer)

Otherwise, teach mother to use Plan A, except:

Dilute any animal milk with equal volume of water or

replace with fermented milk product such as yoghurt

Assure full RENI by giving 6 meals a day, thick cereal

and added oil, mixed vegetables, meat, fish

Follow up in 5 days

Diarrhea has not stopped Refer to hospital

Diarrhea has stopped:

(1) Use same food for regular diet
(2) After 1 week gradually resume usual milk
(3) Give extra meal each day for at least 1 month

3.

4.

Severe undernutrition

Do not attempt rehydration

Refer to hospital for management

Give ORS 5 mL/kg/hr

Fever

Give Paracetamol q4 for Temperature 39.0C or greater

If there is Falciparum malaria in the area, and child has

fever of 38.0C and above OR history of fever in the past 5
days: Give antimalarial

Other Common Antimicrobials for Diarrhea

CAUSE
Cholera

ANTIBIOTIC OF CHOICE
Tetracycline
Children: 12.5 mg/kg QID for 3
days
Adults: 500 mg QID for 3 days

ALTERNATIVE(S)
Furazolidone
Children: 1.25 mg/kg QID for 3 days
Adults: 100 mg QID for 3 days
Or

Or
Doxycycline
Adults: 300 mg OD for 3 days

Amoebiasis

Metronidazole
Children: 10 mg/kg TID for 5 days
Adults: 750 mg TID for 5 days

Giardiasis

Metronidazole
Children: 5 mg/kg TID for 5 days
Adults: 250 mg TID for 5 days

Trimethoprim (TMP)
Sulfamethoxazole (SMX)
Children: TMP 5 mg/kg + SMX 25
mg/kg BID for 5 days
Adults: TMP 160 mg + SMX 800 mg
BID for 3 days
Severe cases:
Dehydroemetine hydrochloride
IM OD for 10 days
PO 1 1.5 mg/kg OD for 5 days
Quinacrine HCl
Children: 2.5 mg/kg TID for 5 days
Adults: 100 mg TID OD for 5 days

References
1.
2.

Dr. Enrique H. Carandangs Diarrheal Diseases and Dehydration from

the Handbook of Medical and Surgical Emergencies, 5th edition
Nelson Textbook of Pediatrics, 19th edition

13 HEPATIC ENCEPHALOPATHY
Definition

State of disordered CNS function resulting from failure of the

liver to detoxify noxious agents of gut origin because of
hepatocellular dysfunction and portosystemic shunting
(Current Medical Diagnosis and Treatment 2014) secondary to
a chronic hepatic pathology or acute hepatic failure

Syndrome of acute hepatic failure manifested as psyhicatric

and neurologic abnormalities with jaundice within 2 to 8 weeks
of onset of symptoms without pre-existing liver disease
(Handbook of Medical and Surgical Emergencies, 5th edition)
Etiology

Viral (Hepatitis)

Drugs diuretics, opioids, hypnotics, sedatives

Chemical Ammonia: most readily identified and measurable

toxin, but is not solely responsible for disturbed mental status

Others surgery, radiation, cancer

Precipitating factors

Azotemia

Electrolyte imbalance hypokalemia, alkalosis

High protein diet

Gastrointestinal bleeding

Hypovolemia

Sedative/tranquilizer

Surgery
Pathogenesis

Normally, ammonia is produced from the breakdown of

dietary amino acids by colonic bacterial flora.

Ammonia is reabsorbed by the portosystemic circulation.

80 to 90% of the total ammonia produced is brought to

the liver where it is converted into Urea.

Urea is released into the circulation and excreted in urine.

The remaining 10 to 20% is metabolized by the kidneys,

heart, and brain.

When more than 60% of hepatic function is lost or when

portosystemic shunting is present, there is failure of ammonia
detoxification into urea.

Ammonia levels escalate but the ability of the kidneys,

heart, and brain to metabolize ammonia remains the
same. Hence hyperammonemia occurs.

Ammonia has multiple neurotoxic effects:

Alters transit of amino acids, water, electrolytes across

astrocytes and neurons

Impairs amino acid metabolism and energy utilization in

the brain

Inhibits
generation
of excitatory
and
inhibitory
postsynaptic potentials
Manifestations

Major features:

Altered consciousness

Personality change

Motor abnormalities

Neuro-ophthalmologic changes

Electroencephalographic changes: slow, high-amplitude,

triphasic waves

West Haven Classification System

GRADE
0

II

III

IV

SYMPTOMS
Undetectable changes in personality, behavior
(+) Minimal changes in memory, concentration,
intellect, coordination
Sleep reversal pattern, hypersomnia, or insomnia
Euphoria, depression, irritability
Mild confusion, slowed ability to do mental tasks
Lethargy, drowsiness
Inappropriate behavior
Disorientation, gross deficits in ability to perform
mental tasks
Somnolence
Aggressive behavior
Severe confusion, unable to perform mental
tasks, amnesia
Coma with or without response to normal stimuli

MOTOR
(-)

EEG
Normal

Tremors

Normal

Asterixis

(+)

Asterixis

(+)

Asterixis

(+)

Diagnosis

Usually clinical characteristic signs, symptoms

Treatment: Reduce ammonia formation
1. Nonabsorbable dissacharides

Lactulose

Mechanism of action:
(1) Digested by colonic bacteria to short-chain fatty
acids resulting to acidification of colon contents
Acidification favors formation of Ammonium
ion (NH4+)which is not absorbable and nontoxic
(2) Also leads to change in bowel flora to decrease
ammonia forming organisms
(3) Catharsis eliminates nitrogenous waste products

Dose:
(1) 30 ml PO tid-qid with maintenance dose
adjusted to produce 3 to 5 soft stools per day
(2) If patient cannot tolerate PO give Lactulose 300
ml added to 700 ml distilled water as retention
enema for 30 to 60 minutes qid to q6h
2. Antibiotics: to control ammonia producing intestinal flora

Alternating administration of:

(1) Neomycin 500 1000 mg q6h PO

Interferes with bacterial protein synthesis by

binding to 30S ribosomal subunit

Adverse effects: ototoxicity, nephrotoxicity

(2) Metronidazole 250 mg q8h PO

Adverse effect: peripheral neuropathy

Inhibits nucleic acid synthesis by disrupting DNA

Alternative:
(3) Rifaximin 550 mg BID PO

Binds to -subunit of bacterial DNA dependent

RNA polymerase

Better safety profile

3. Control GI bleeding and purge blood from the GIT

Magnesium citrate 120 ml PO

Nasogastric tube every 3 4 hours

4. Diet

Dietary protein restriction

No longer recommended by current studies because

malnutrition outweighs the benefits of restriction

Most patients found to be able to tolerate high

protein diets

For those unable to tolerate protein shift to

vegetable sources of protein
Supportive measures
1. Fluid/electrolyte replacements
2. Oxygen inhalation
3. Monitor urinary output, CVP, vital signs
Complications

Coagulation defect, leading to bleeding

Predisposed to infections

Respiratory defects, leading to hypoxemia

Hypovolemia leading to tubular necrosis then renal failure

Cerebral edema leading to encephalopathy

References
1.
2.
3.

Handbook of Medical and Surgical Emergencies, 5th edition

The Washington Manual of Medical Therapeutics 33rd edition
Current Diagnosis and Treatment: Emergency Medicine, 6th edition

14 HYPERTENSIVE URGENCIES AND EMERGENCIES

Definitions

Hypertension presence of blood pressure (BP) elevation to a

level that places patients at increased risk for target organ
damage in several vascular beds including the retina, brain,
heart, kidneys, and large conduit arteries
Normal BP
Prehypertension
Stage 1
Stage 2

DBP
< 80 mmHg
80 89 mmHg
90 99 mmHg
> 100 mmHg

Hypertensive Crisis

Includes hypertensive urgencies and emergencies

Usually develops in patients with previous history of

elevated BP but may arise in previously normotensive

Severity correlates with absolute level of BP elevation and

rapidity of development (autoregulatory mechanisms
have not had sufficient time to adapt)

Definition

Precipitating
settings

SBP
< 120 mmHg
120 139 mmHg
140 159 mmHg
> 160 mmmHg

URGENCY
Severely elevated BP
(DBP > 120 mmHg) in
a patient with no
symptoms, signs, or
laboratory findings of
end-organ damage

Treatment
BP reduction

Antihypertensive
agents

Accelerated HTN SBP > 210 mmHg and DBP

> 130 mmHg with headaches, blurred vision,
or focal neurologic symptoms
Malignant HTN accelerated HTP with
papilledema
Hypertensive encephalopathy
Intracerebral Hemorrhage
Unstable Angina Pectoris
Acute Myocardial Infarction
Acute LV failure with pulmonary edema
Dissecting aortic aneurysm
Progressive renal failure
Eclampsia

Determinants of arterial pressure

Cardiac
output

Stroke
volume
Heart rate

Arterial
pressure
Peripheral
resistance

EMERGENCY
Reduction of 20 to 25% in MAP [(2 DBP +
SBP)/3] within 1 hour to prevent or minimize
end-organ damage
Avoid rapid, severe drops in BP because
Watershed Cerebral Infarction can occur

EMERGENCY
Severely elevated blood pressure (SBP > 210
mmHg and DBP > 130 mmHg) responsible for
symptoms, signs, or laboratory evidence of
end-organ damage

Optic disk edema

Severe perioperative
hypertension
Rebound from abrupt
cessation of
adrenergic inhibiting
drugs

URGENCY
Within 24 hours

Vascular
structure

Clonidine 0.2 mg PO
followed by 0.1 mg
every hour until BP is
controlled
Captopril 12.5 25
mg PO or
Labetalol 200 400
mg PO

If possible, admit to Intensive Care Unit and

consider placing an Intra-arterial line for
constant BP monitoring
Nitroprusside potent vasolidator
Lowers BP in seconds
Insert intra-arterial line to ensure over titration
leading to hypoperfusion does not occur
Continuous IVI 0.5 10 g/kg/min
Nitroglycerin for situations wherein
Nitroprusside is relatively contraindicated (i.e.
Severe coronary insufficiency, advanced
renal or hepatic disease)
Labetalol combination and blocker
IV bolus 20-80 mg over 2 minutes q5-10m
May be doubled every 10 minutes until BP
reduction achieved
Max total dose of 300 mg
Hydralazine vasodilator that may be used
in pregnancy since it also increases uterine
blood flow
IV 10 20 mg every 15 30 mins
Continuous IVI 1.5 5.0 g/kg/min
Fenoldopam dopaminergic agonist useful
in renal insufficiency or failure as alternative
to Nitroprusside (Cyanide toxicity)
Continuous IVI 0.1 0.3 g/kg/min
Enalaprilat IV ACEI useful for congestive
heart failure, stroke, as alternative to
Nitroprusside
0.6255 mg/dose over 5 mins q6h
Phentolamine alpha-adrenergic receptor
blocker useful in Pheochromocytoma crisis
Continuous IVI 50 300 g/kg/min
Diazoxide potassium channel activator that
relaxes smooth muscles to decrease PVR,
increase HR and CO, useful for renal failure
IV bolus 20 80 mg q5-10 mins
Nicardipine CCB useful in post-op HTN
Nifedipine CCB useful in angina

Furosemide loop diuretic which blocks sodium reabsorption

in TAL of Henle by inhibiting Na/K/2 Cl cotransporter, effective
especially in renal insufficiency

Vascular
function

Etiology

90% of patients have Primary or Essential Hypertension

10% of patients have Secondary Hypertension

Renal parenchymal disease

Renovascular disease

Pheochromocytoma

Cushings Syndrome

Primary Hyperaldosteronism

Coarctation of the aorta

Obstructive sleep apnea

Management
Laboratories and ancillaries to identify patients with possible target
organ damage assess cardiovascular risk and provide baseline
for monitoring adverse effects of therapy
1. Urinalysis
2. Hematocrit
3. Plasma glucose
4. Serum potassium
5. Serum creatinine
6. Calcium
7. Uric Acid
8. Fasting lipid levels
9. Electrocardiogram
10. Chest X-ray
11. Echocardiography

References
1.
2.
3.
4.

Dr. Adoracion Nambayan-Abads Hypertensive Crises: Emergencies

and Urgencies from the Handbook of Medical and Surgical
Emergencies, 5th edition
The Washington Manual of Medical Therapeutics 33rd edition
Current Diagnosis and Treatment: Emergency Medicine, 6th edition
Acute Care Evaluation and Management of Hypertensive Emergencies,
Emergency Medicine Cardiac Research and Educational Group
International

20 HEMOPTYSIS
Definition[1,2]

Expectoration of the blood from the lungs or bronchial tubes

or coughing out blood in gross amounts or fine streaks from a
source below the glottis (Steadmans Medical Dictionary)

Massive hemoptysis

Occurs in 5% of cases

200 to 600 mL of blood expectorated in 24 hours

Clinically, any bleeding that results in the impairment of

lung function and gas exchange

Originates from a bronchial artery in 90% of cases

20% fatality rate

Causes[1]
1.

2.

3.

4.

5.

6.

7.

8.

9.

Infections
1.1. Bronchiectasis
} Indolent productive cough
1.2. Acute/chronic bronchitis
} Acute fever, cough, bloody sputum
1.3. Necrotizing pneumonias
1.4. Pulmonary Tuberculosis fever and night sweats
1.5. Lung abscess
1.6. Fungal infections (Aspergilloma)
1.7. Amoebic liver abscess (Pleuro-pneumonic complications)
1.8. Paragonimiasis
Neoplasms weight loss and change in cough
2.1. Primary
2.1.1. Bronchial adenoma
2.1.2. Carcinoid tumor
2.1.3. Bronchial cancer
2.2. Metastatic
2.2.1. Choriocarcinoma
2.2.2. Osteogenic carcinoma
Cardiovascular conditions
3.1. Mitral stenosis chronic dyspnea and minor hemoptysis
3.2. Acute pulmonary edema
3.3. Aortic aneurysm rupture in a bronchus
3.4. Atrioventricular malformations
Thromboembolic dyspnea and pleuritic chest pain
Pulmonary infarction from:
4.1. Deep Venous Thrombosis
4.2. Septic emboli
4.3. Fat embolism
Trauma
5.1. Blunt/crushing injuries/pulmonary contusion
5.2. Penetrating injuries from rib fractures
5.3. Bullet or bladed weapons
Iatrogenic
6.1. Related to maintenance of airway patency (endotracheal and
tracheostomy tubes both tip and balloon related)
6.2. Related to hemodynamic monitoring of the critically ill
pulmonary catheter related via:
6.2.1. Perforation/rupture
6.2.2. Pulmonary infarction
6.3. Related to diagnostic procedures:
6.3.1. Bronchoscopy with biopsy (transbronchial biopsy,
transbronchial lung biopsy)
6.3.2. Percutaneous lung biopsy
Massive Hemoptysis in the ICU
7.1. Hemoptysis complicating a systemic disease
7.2. Hemoptysis complicating a therapeutic or diagnostic procedure
7.3. Trauma from vigorous suctioning
Miscellaneous
8.1. Anticoagulation
8.2. Thrombocytopenia
8.3. Disseminated Intravascular Coagulation
8.4. Aspiration (Foreign bodies, gastric content)
8.5. Blood dyscrasias
8.6. Auto-immune diseases: Good Pastures Syndrome, SLE, Wegener
granulomatosis)
8.7. Idiopathic (Pulmonary hemosiderosis)
Cryptogenic Hemoptysis
9.1. Found in 20% of cases
9.2. Undetermined
cause
despite
extensive
evaluation
(bronchoscopy, CT scan, bronchogram)

Clinical Manifestations[1]

Dependent on primary disease, site, degree, and rate of

hemorrhage

True hemoptysis vs. Epistaxis

True hemoptysis
1. Bleeding below the glottis
2. Follows coughing spells

Epistaxis
1. Bleeding above the glottis (upper airway source)
2. Sensation of pooling of blood in the throat or need to
clear the throat before bleeding
Minor hemoptysis or blood-streaked sputum

With/without discomfort/bubbling sensation over chest

If with repeated episodes consider massive hemorrhage

Massive hemoptysis

Asphyxiation from flooding of the airways resulting to

acute respiratory failure
1. Tachypnea
5. Changes in sensorium
2. Dyspnea
6. Coma
3. Audible rhonchi 7. Death
4. Cyanosis

Hemodynamic alterations from acute blood loss

4. Rapid pulse
1. Pallor
2. Dizziness
5. Cold clammy skin
3. Hypotension

Diagnosis[1]

Goals

Determine site, cause, degree of hemorrhage

Assess hemodynamic, ventilator, and oxygenation status

Determine need, feasibility, application of appropriate

medical and surgical interventions

Work-up

History and PE may suggest etiology

ENT examination to rule out upper airway source of

bleeding
1. Rhinoscopy
2. Nasopharyngeal and laryngeal endoscopy

Chest X-ray to determine site, etiology, extent of disease

CBC with platelet and coagulation studies

Gross, bacteriologic cytologic examinations of sputum

(character,
appropriate
smears/cultures,
and
cytopathology)

Arterial blood gas: assess oxygenation, ventilator, and

acid-base status

Bronchoscopy: can be both diagnostic and therapeutic

1. Fiber-bronchoscope for mild or moderate bleeding
2. Rigid scope for massive bleeding better visibility,
suctioning, airway control

Specific imaging tools e.g. High resolution CT scan for tiny

bronchial/pulmonary lesions or interstitial lung diseases
Treatment[1]

Existing clinical practice guidelines are disease specific

Management of MILD HEMOPTYSIS
Bed rest
Antitussives
Chest X-ray
(CT scan if indicated)

Mild hemoptysis

Persistent bleeding

Fiber bronchoscopy

Disease specific treatment

Positive

Tx: Medical/Surgical

Negative

CT scan or Bronchography
Negative

Conservative treatment

Positive

Tx: Medical/Surgical

Minor Hemoptysis

No specific intervention required for small amounts of blood in

the sputum other than that directed toward primary disease
and watchful waiting

Non-pharmacologic:

Avoid strenuous/competitive activities

Stop any anticoagulants and anti-platelets

Avoid chest percussion or vigorous physiotherapy

May
be
initially
controlled
during
diagnostic
bronchoscopy

Pharmacologic:

Disease specific treatment ASAP

Cough suppressants: optional, use with caution

Examples[3]
1. Dextromethorphan levorphanol derivative, has
central action on the cough center in the medulla
2. Codeine phenantrene-derivative opiate agonist
that binds to opiate receptors in the CNS to cause
analgesia, has central action on the cough center in
the medulla
3. Benzonatate non-narcotic antitussive with local
anesthetic effect on stretch receptors in respiratory
passages and lungs that reduces cough reflex
Management of MASSIVE HEMOPTYSIS (200 600 ml/24 hours)
ICU
Lie on side affected/Head
down position

Massive hemoptysis

History, Physical Examination

Assess oxygenation/ventilation status
(Intubate/ventilate for impending respiratory failure)
Assess hemodynamic status
(Crystalloids, Colloids, Blood)
Chest X-ray (CT scan may be indicated)
Bronchoscopy (rigid or fiberscope)

Source identified

No identifiable source

Suction/lavage
Selective Endobronchial Intubation
Endobronchial Tamponade
Double Lumen Endotracheal Tube

Surgery
indicated

Surgery
contraindicated
or patient refuses

Resectional
surgery

Arterial
embolization

Source identified

Bronchial
arteriography

No identifiable source

Pulmonary
arteriography

MASSIVE HEMOPTYSIS

Real danger in massive hemoptysis is asphyxia not blood loss

Monitor/maintain airway patency and adequacy of

ventilation

Patient in head down position with bleeding side

dependent to avert aspiration into the opposite lung

Intubate,
oxygenate,
mechanically
ventilate
for
impending respiratory failure

Initial volume resuscitation

Crystalloid or colloid infusions initially

Whole blood transfusions for recurrent moderate to severe

bleeding

Localize, isolate, and arrest the hemorrhage

Bronchoscopy (rigid) to visualize and pack bleeding site

Appropriate use of Fogarty embolectomy catheter for

balloon occlusion

Use of Carlens double lumen tube allows isolation and

separate ventilation of each lung

Resectional surgery for localized disease with recurrent

massive bleeding and failed medical treatment

Selective arterial embolization for diffuse disease and for

patients who refuse surgery

Initiate disease specific treatment

Consider resectional surgery or selective arterial

embolization after tamponade in patients with > 400 ml of
expectorated blood in the first 3 hours or > 600 ml within
24 hours
References
1.
2.
3.

Hemoptysis by Dr. Bernardo D. Briones, Handbook of Medical and

Surgical Emergencies
Tintinallis Emergency Medicine: A Comprehensive Study Guide
MIMS Drug Information System Philippines

26 THYROID STORM / THYROTOXIC CRISIS by: toxic JI

Essentials of Diagnosis
Typical
stigmata
of
hyperthyroidism,
thyromegaly,
ophthalmopathy, tremor, stare, diaphoresis, and agitation
Fever (usually)
Tachycardia (out of proportion to fever) often with associated
atrial arrhythmias
Mental status changes ranging from confusion to coma
Introduction/Definition
Thyroid hormone affects all organ systems and is responsible
for increasing metabolic rate, heart rate, and ventricle
contractility, as well as muscle and central nervous system
excitability.
Two major types of thyroid hormones are thyroxine and
triiodothyronine.
o
Thyroxine is the major form of thyroid hormone.
o
The ratio of thyroxine to triiodothyronine released in the
blood is 20:1.
o
Peripherally, thyroxine is converted to the active
triiodothyronine, which is three to four times more potent
than thyroxine.
Hyperthyroidism refers to excess circulating hormone resulting
only from thyroid gland hyperfunction, whereas thyrotoxicosis
refers to excess circulating thyroid hormone originating from
any cause (including thyroid hormone overdose).
Thyroid storm is the extreme manifestation of thyrotoxicosis. This
is an acute, severe, life-threatening hypermetabolic state of
thyrotoxicosis caused either by excessive release of thyroid
hormones causing adrenergic hyperactivity or altered
peripheral response to thyroid hormone following the
presence of one or more precipitants.
The mortality of thyroid storm without treatment is between
80% and 100%, and with treatment, it is between 15% and 50%.
In the case of thyroid storm, the most common underlying
cause of hyperthyroidism is Graves disease.
It occurs most frequently in young women (10 times more
common in women compared with men) at any age
Causes
MOST COMMON: Thyroid storm usually occurs when an
already thyrotoxic patient (Graves disease, toxic multinodular
goiter, and toxic adenoma are most common) suffers a serious
concurrent illness, event, or injury.
During thyroid storm, precipitants such as infection, stress,
myocardial infarction, or trauma will multiply the effect of
thyroid hormones by freeing thyroid hormones from their
binding sites or increasing receptor sensitivity.

Clinical Manifestations
The diagnosis of thyroid storm should be made clinically.
Often a history of partially treated hyperthyroidism or signs of
thyroid disease such as thyromegaly, proptosis, stare, myopathy,
or myxedema can be found.
The diagnosis should be made in the patient with a probable
history of thyroid disease, which rapidly decompensates in the
setting of fever, tachycardia, gastrointestinal symptoms, and
mental status change.

Fever may exceed 40C (104F). This is due to the catabolic

state of thyrotoxicosis
Cardiac findings usually include a friction rub or systolic flow
murmur, and either sinus or supraventricular tachycardia. The
heart rate is often characterized as out of proportion to fever.
Mental status changes are also common.
Gastrointestinal symptoms include nausea, vomiting, diarrhea,
and abdominal paincan mimic an acute abdomen.
Neuromuscular findings such as agitation, tremor, generalized
weakness (especially in the proximal muscles), and periodic
paralysis are also seen.
Dermatologic findings include warm, moist, smooth skin and
palmar erythema.
Apathetic hyperthyroidism is important to consider in the
elderly population. With advanced age and other comorbid
conditions, the classic symptoms and signs of thyroid storm
and thyrotoxicosis may be absent.

Ancillary Diagnostic Findings

Draw blood samples to test for free T4, T3, and TSH (thyroidstimulating hormone) and serum cortisol levels.
A complete blood count, serum electrolytes, glucose renal
and hepatic function tests, and ABG analysis should be
performed;
Obtain cultures of the blood, urine, and possibly sputum; chest
X-ray and ECG are indicated to look for precipitating causes
or complications.
Cranial CT scan is indicated for delirious or comatose patients.
Previous abnormal thyroid function tests may suggest a
preexisting thyrotoxicosis. TFTs may be misinterpreted based on
levels of thyroid binding globulin.
TSH will be markedly low in most patients with thyroid storm or
thyrotoxicosis. Free thyroxine (T4) will be elevated, again similar
to thyrotoxicosis.
Electrolyte and glucose abnormalities may also be present
due to gastrointestinal losses, dehydration, physiologic stress,
and fever
The ECG is usually abnormal; common findings are sinus
tachycardia, increased QRS interval and P wave voltage,
nonspecific STT wave changes, and atrial dysrhythmias,
usually atrial fibrillation or flutter

Emergency Measures
SHORCUT:
Treatment aims are as follows:
1. Supportive care
2. Inhibition of new hormone synthesis
3. Inhibition of thyroid hormone release
4. Peripheral -adrenergic receptor blockade
5. Preventing
peripheral
conversion
of
triiodothyronine
6. Treat precipitating event

6.

thyroxine

to

LONGCUT:
1. Supportive care
General: oxygen, cardiac monitoring Fever: external
cooling; acetaminophen 325650 milligrams PO/PR every
46 h (aspirin is contraindicated because it may increase
free thyroid hormone)
Volume replacement: is commonly indicated with at least
1 L of normal saline or lactated Ringer's solution in the first
hour due to volume depletion from fever.
Nutrition: glucose, multivitamins, thiamine, including folate
can
be
considered
(deficient
secondary
to
hypermetabolism)
Cardiac decompensation (atrial fibrillation, congestive
heart failure): rate control and inotropic agent, diuretics,
sympatholytics as required
2.

Inhibition of new thyroid hormone synthesis with thionamides

Thionamides are the standard first-line agents to treat
thyroid storm.

Methimazole. (Avoid methimazole for pregnant women

in first trimester as it can cause teratogenic effect. It can
only be used in second and third trimester of pregnancy.)

PTU, (PTU also blocks peripheral conversion of thyroxin to

triiodothyronine.) (PTU is used for pregnant women in first
trimester. PTU also has a boxed warning issued by the U.S.
Food and Drug Administration in 2010 regarding its rare
but severe side effect toward liver function.
Methimazole is preferred as first-line treatment unless
contraindicated.)

3.

Inhibition of thyroid hormone release

(at least 1 h after step 2)
Iodine therapy is an adjunct to the thionamides.
It should not be given until at least 12 hours after PTU or
methimazole is administered. Early administration can
promote further hormone production, thus worsening
hyperthyroidism.
Several forms are available such as potassium iodide (SSKI,
35 mg/drop) 5 drops PO every 6 hours or Lugol's solution 8
drops every 6 hours.
If iodine allergy is a concern, lithium carbonate can be
given instead

4.

-Adrenergic receptor blockade

-Adrenergic agonists such as propranolol block the
peripheral effects of excess thyroid hormone.
Beta blockers may be especially attractive in cases of
atrial fibrillation with rapid ventricular response

5.

Preventing
peripheral
conversion
of
thyroxine
to
triiodothyronine

Corticosteroids inhibit peripheral conversion of T4 to T3

and block the release of hormone from the thyroid
gland.

In addition, they treat the relative adrenal insufficiency

that may be present

Intravenous hydrocortisone, 100 mg every 8 hours, is the

treatment
of
choice
for
concurrent
adrenal
insufficiency; however, dexamethasone, 0.1 mg/kg
intravenously every 8 hours, may be given

Treat precipitating event

All triggers of thyroid storm should be searched and

treated accordingly (infection, myocardial infarct,
diabetic ketoacidosis, etc.).

29 ANIMAL BITES

In small children, the bite is usually provoked and tends to be

on the hands or face
If unprovoked, the bite is usually in the legs, thighs, or buttocks
Dog bites tend to be crushing injuries or puncture wounds
rather than clean, sharp lacerations
Complications:

Wound infection or abscess

Fractures

Septicemia

RABIES

Rapidly progressive, acute infectious disease of the central

nervous system in humans and animals caused by infection
with the Rabies virus normally transmitted from animal vectors

Rabies virus

Family Rhabdoviridae

Lyssavirus: causes serious neurologic disease when

transmitted to humans

Vesiculovirus: causes vesiculation and ulceration in cattle,

horses, and other animals and causes self-limited, mild
systemic illness in humans
Pathogenesis

Negri body

Most characteristic pathologic finding

Eosinophilic cytoplasmic inclusions in brain neurons

composed of virus proteins and viral RNA

Common in Purkinje cells of Cerebellum and

Pyramidal neurons of Hippocampus
Centrifugal spread along sensory and autonomic nerves to
other tissues including:

Salivary glands: virus replicates in acinar cells and

secreted in saliva

Heart

Adrenal glands

Skin

6.

Clinical manifestations
Phase
Incubation
Prodrome

Typical
duration
20 90 d
2 10 d

Encephalitic
(80%)

27d

Paralytic
(20%)
Coma, death

2 10 d

Symptoms and Signs

None
Fever, malaise, anorexia, nausea, vomiting,
paresthesias, pain, pruritus at wound site
Anxiety, agitation, hyperactivity, bizarre
behavior, hallucinations, autonomic
dysfunction, hydrophobia
Flaccid paralysis in limbs, progressing to
quadriparesis with facial paralysis

0 14 d

Diagnosis
1. Rabies virus specific antibodies (+) serum neutralizing
antibodies to rabies diagnostic in previously unimmunized but
may not develop until late in disease
2. RT-PCR amplification highly sensitive and specific; saliva, CSF,
skin, brain tissue may be used
3. Direct fluorescent antibody testing highly sensitive and
specific; can be performed quickly and applied to skin
biopsies and brain tissue
Prognosis

Almost uniformly fatal disease but always preventable with

appropriate postexposure therapy during early incubation
period
Treatment

1.
2.
3.
4.

5.

Incubation period (interval between exposure and onset of

clinical disease) 20 to 90 days
During incubation, the virus is present or close to site of
inoculation
In muscles, virus binds to nicotinic acetylcholine receptors on
postsynaptic membranes at neuromuscular junctions
Virus spreads centripetally along peripheral nerves toward
CNS at 250 mm/d via retrograde fast axonal transport to spinal
cord or brainstem
Virus rapidly disseminates to other regions of CNS via fast
axonal transport along neuroanatomic connections

Neurons are prominently infected

Babes nodules microglial nodules

Guidelines

Inquire about epidemiology of rabies in local community

Unprovoked bites by wild or stray animals will always

require immunization with RIg and a complete course of
rabies vaccine

Scratches by the claws of rabid animals are dangerous

because animals lick their claws. Saliva applied to a
mucosal surface may be infectious
Also give Tetanus immunization depending on patients
immunization status

SAN LAZARO HOSPITAL GUIDELINES

What are the guidelines for Rabies Post-Exposure Prophylaxis?
1. Apply local wound treatment immediately to exposures of all
types of category.

Vigorously wash and flush with soap or detergent and

water for 10 minutes

Apply alcohol, povidone iodine, or any antiseptic

AVOID suturing

DO NOT apply ointment, cream, or dressing

Apply antimicrobials (Co-amoxiclav, Cefuroxime axetil)

for the following conditions:

Frankly infected wounds

All category III bites

Give Anti-Tetanus immunization if indicated

2. Assess the category of the wound and apply recommended
treatment.
CATEGORY
CATEGORY I
Feeding or touching an animal
Licking of intact skin
Exposure to patient with S/S of rabies by
sharing or eating or drinking utensils*
Casual contact to patient with S/S of
rabies*

CATEGORY II
Nibbling/nipping of uncovered skin with
bruising
Minor scratches/abrasions WITHOUT
bleeding*
Licks on broken skin
*Include wounds that are INDUCED to
bleed

CATEGORY III
Transdermal bites or scratches
*Include puncture wounds, lacerations,
avulsions
Contamination of mucous membrane
with saliva (i.e. licks)
Exposure to rabies patient through bites,
contamination of mucous membranes or
open skin lesions with body fluids (except
blood/feces)
Handling of infected carcass or ingestion
of raw infected meat
All Category II exposures on head and
neck area

MANAGEMENT

Local wound treatment

NO vaccine or RIG needed
*Consider Pre-exposure vaccination

Start vaccine immediately

1. COMPLETE regimen until Day 28/30 if:
Animal is rabid, killed, died, or
unavailable for 14 day
observation and examination
Animal under observation died
within 14 days, was IFAT positive,
or no IFAT testing was done, or
had signs of rabies
2. COMPLETE regimen until Day 7 if:
Animal is alive and remains
healthy after 14 days observation
Animal died within 14 days, was
IFAT negative, and without any
signs of rabies
Start vaccine and RIG immediately
1. COMPLETE regimen until Day 28/30 if:
Animal is rabid, killed, died, or
unavailable for 14 day
observation and examination
Animal under observation died
within 14 days, was IFAT positive,
or no IFAT testing was done, or
had signs of rabies
2. COMPLETE regimen until Day 7 if:
Animal is alive and remains
healthy after 14 days observation
Animal died within 14 days, was
IFAT negative, and without any
signs of rabies

ACTIVE IMMUNIZATION PRODUCTS

Injections should be given IM (2.5 IU) or ID (0.5 IU) on:

Adults: deltoid area of each arm

Infants: anterolateral aspect of the thigh

NEVER in the gluteal area because absorption is

unpredictable

Types:
1. Purified Vero Cell Rabies Vaccine (PVRV) [0.5 ml]
2. Purified Chick Embryo Cell Vaccine (PCECV) [1.0 ml]

Vaccination regimen:

Standard Intramuscular Schedule (1-1-1-1-1):

D0D3D7D14D28/30

Abbreviated multisite schedule IM (2-1-1):

2 D01 D71 D21

Abbreviated multisite schedule ID (2-2-2-0-2):

2 D02 D32 D70 D14 2 D30

Previously immunized animal bite patients

Special conditions:

Pregnancy and infancy are NOT contraindications

Babies born of rabid mothers should be given vaccine

and RIG as early as possible

Patients taking chloroquine, anti-epileptics, systemic

steroids, and alcoholic patients should be given standard
IM regimen

All Category II and III immunocompromised patients

should receive standard IM regimen and RIG
Pre-exposure vaccination (D0D7D21/28) is recommended
for individuals at high risk of exposure:

Rabies diagnostic laboratories

Veterinarians and veterinary students

Animal handlers

Health care workers of rabies patients

Rabies control personnel

Children 2 to 10 years old

Field workers

INTERVAL FROM LAST DOSE

Less than 1 month
1 5 months
More than 6 months 3 years
More than 3 years

VACCINATION (ID or IM)

No booster dose
1 booster
2 booster doses (D0, D3)
Full course of active immunization

PASSIVE IMMUNIZATION PRODUCTS (RIG)

Given to provide immediate neutralizing antibodies to cover

the gap until the appearance of vaccine detectable
antibodies

Total computed RIG should be infiltrated around and into the

wound as much as anatomically feasible even if the lesion has
healed

Remaining RIG should be administered deep IM at a site

distant from the site of vaccine injection

Types:
1. Human Rabies Immune Globuline (HRIG) from plasma of
human donors; Dose = 20 IU/kg
2. Highly Purified Antibody Antigen Binding Fragments
(F(ab)2) from equine rabies immune globuline (ERIG);
Dose = 40 IU/kg
3. Equine Rabies Immune Globulin from horse serum; Dose
= 40 IU/kg

References
1. Handbook of Medical and Surgical Emergencies, 6th edition
2. Longo, D.L., Fauci, A.C., Kasper, D.L, et al. (2013). Harrisons
Principles of Internal Medicine, 18th edition. McGraw-Hill
Companies Inc.: New York.
3. San Lazaro Hospital Rotation notes

30 TETANUS by: toxic JI

Definition:
Tetanus is an acute, often fatal disease caused by wound
contamination
with
Clostridium
tetani,
a
motile,
nonencapsulated anaerobic gram-positive rod.
Pathophysiology:
C. tetani exists in either a vegetative or a spore-forming state.
The spores are ubiquitous in soil and in animal feces and are
extremely resistant to destruction, surviving on environmental
surfaces for years.
C. tetani is usually introduced into a wound in the spore-forming,
noninvasive state but can germinate into a toxin-producing,
vegetative form if tissue oxygen tension is reduced.
Factors such as the presence of crushed, devitalized tissue, a
foreign body, or the development of infection favor the growth
of the vegetative, toxin-producing form of C. tetani.
C. tetani produces two exotoxins.
1st toxin: Tetanolysin
o
Which appears to favor the expansion of the bacterial
population, and
2nd toxin: Tetanospasmin
o
A powerful neurotoxin that is responsible for all the clinical
manifestations of tetanus. Tetanospasmin is one of the
most potent toxins known
o
Although the infection caused by C. tetani remains
localized to the site of injury, tetanospasmin reaches the
nervous system by hematogenous spread of the exotoxin
to peripheral nerves and by retrograde intraneuronal
transport.
o
Tetanospasmin acts on the motor end plates of skeletal
muscle, in the spinal cord, brain, and sympathetic nervous
system. This extremely potent exotoxin prevents the release
of the inhibitory neurotransmitters glycine and aminobutyric acid (GABA) from presynaptic nerve
terminals, releasing the nervous system from its normal
inhibitory control.
All of the clinical manifestations of tetanus are
secondary to tetanospasmin, and there is no personto-person transmission of the disease
Clinical Features:
Tetanus results in generalized muscular rigidity, violent
muscular contractions, and autonomic nervous system
instability.
Wounds that become contaminated with toxin-producing C.
tetani are most often puncture wounds, but contaminated
wounds range from deep lacerations to minor abrasions.
No wound is identified in up to 10% of patients with tetanus.
Tetanus can also develop after surgical procedures, otitis
media, or abortion and can develop in injection drug users
from contaminated heroin and in neonates through infection
of the umbilical stump.
The incubation period for tetanus ranges from <24 hours to
more than 1 month. Shorter incubation periods are associated
with more severe disease and a worse prognosis for recovery.
Clinical tetanus can be categorized into three forms:
generalized, cephalic, and local. The different categories of
clinical tetanus depend on the population of neurons involved.
1.

Generalized tetanus
o
The most common form of the disease and
accounts for approximately 80% of cases.
o
The most frequent presenting complaints of
patients with generalized tetanus are pain and
stiffness in the masseter muscles (lockjaw).
o
Nerves with short axons are affected initially, so
symptoms appear first in the facial muscles, with
descending progression to the muscles of the
neck, trunk, and extremities.
o
The transition from muscle stiffness to rigidity
leads to the development of trismus and the

2.

3.

characteristic facial expression: risus sardonicus

(sardonic smile).
o
Reflex convulsive spasms and tonic muscle
contractions
are
responsible
for
the
development of dysphagia, opisthotonus flexing
of the arms, clenching of the fists, and extension
of the lower extremities.
o
The mental status is normal, an important
consideration in differentiating tetanus from
other disorders. Patients remain conscious and
alert.
o
Neonatal tetanus, a form of generalized tetanus,
develops in infants born to inadequately
immunized mothers, frequently after unsterile
treatment of the umbilical cord stump. Infants
with neonatal tetanus are weak, irritable, and
have an inability to suck. Symptoms are evident
during the second week of life.
Cephalic tetanus
o Follows injuries to the head or occasionally otitis
media and results in dysfunction of the cranial
nerves, most commonly the seventh.
o It has a poor prognosis.
Local tetanus
o Manifested by rigidity of muscles in proximity to
the site of injury and usually resolves completely
after weeks to months.
o Local tetanus may progress to the generalized
form of the disease.
o Approximately 1% of the cases are fatal.

Workups
Tetanus is diagnosed clinically.
Most patients who develop the disease have an unknown or
inadequate immunization history.
Wound culture is of limited value, because C. tetani may be
cultured from wounds in the absence of clinical disease and
may not be recovered in patients with documented tetanus
Emergency Management
Admit patients with tetanus to the intensive care unit.
Respiratory compromise requires immediate neuromuscular
blockade and orotracheal intubation.
Minimize environmental stimuli to prevent the precipitation of
reflex convulsive spasms.
A. Tetanus Immunoglobulin 1st step! (wound management is 2nd
step only)
Human tetanus immunoglobulin (TIG) neutralizes circulating
tetanospasmin and toxin in the wound but not toxin that is
already fixed in the nervous system.
Even though TIG does not ameliorate the clinical symptoms of
tetanus, it significantly reduces mortality.
3000 to 6000 units IM is the usual recommended dose
Administered in a separate syringe and opposite the site of
tetanus toxoid administration.
At least a portion of the dose should be administered around
the wound itself.
IG should be given before wound debridement, because
exotoxin may be released during wound manipulation.
B. Wound Management
Initial care involves identifying and debriding the wound to
improve the oxidation-reduction potential of infected tissue
and to prevent further toxin production.
Antibiotics are of limited value but are traditionally
administered. Parenterally administered metronidazole is the
antibiotic of choice.
Do not give penicillin because it is a centrally acting GABA
antagonist that may potentiate the effects of tetanospasmin.

C. Muscle Relaxants
Tetanospasmin prevents neurotransmitter release at inhibitory
interneurons, and therapy of tetanus is aimed at restoring
normal inhibition.
The benzodiazepines are centrally acting inhibitory agents
that have been used extensively for this purpose.
Give the water-soluble agent, midazolam, for muscle
relaxation. 1st Line!
D. Neuromuscular Blockade
To control ventilation and muscular spasms as well as to
prevent
fractures
and
rhabdomyolysis,
prolonged
neuromuscular blockade may be required in the treatment of
tetanus.
Succinylcholine an be given for emergency airway control,
whereas vecuronium a good option for prolonged blockade
because of minimal cardiovascular side effects.
E. Treatment of Autonomic Dysfunction
1st Line- Magnesium sulfate inhibits the release of epinephrine
and norepinephrine from the adrenal glands and adrenergic
nerve terminals, eliminating the source of catecholamine
excess in tetanus.
Labetalol, the combined - and -adrenergic blocking agent
has been used successfully in treating the manifestations of
sympathetic hyperactivity of tetanus.
Morphine sulfate reduces sympathetic -adrenergic tone and
central sympathetic efferent discharge and produces
peripheral arteriolar and venous dilatation.
Clonidine, a central 2-receptor agonist, has also been used to
manage tetanus-induced cardiovascular instability.
F. Active Immunization
Patients who recover from tetanus must receive active
immunization, because the disease does not confer immunity.

Adsorbed tetanus toxoid (0.5 mL) should be administered IM

at the time of presentation and at 6 weeks and 6 months after
injury.
2 forms:
o Td (tetanus-dipththeria) - to patients 7 years of age
o DTap (tetanus toxoid, reduced diphtheria toxoid, and
acellular pertussis vaccine) - to children <7 years of age.
Tetanus immunization should be administered to unimmunized
or inadequately immunized pregnant women. Because Tdap
has not been tested in pregnancy, Td is preferred in pregnant
adolescents and adults.

32 STROKE by toxic JI
(2 parts siya. ang haba! I tried to make it as short as possible)

Stroke is a cerebrovascular disorder resulting from impairment

of cerebral blood supply by occlusion (eg, by thrombi or
emboli) or hemorrhage.
It is characterized by the abrupt onset of focal neurologic
deficits.
Thus, the definition of stroke is clinical, and laboratory studies
including brain imaging are used to support the diagnosis.
The clinical manifestation depends on the area of the brain
served by the involved blood vessel.
Stroke is the most common serious neurologic disorder in
adults and occurs most frequently after age 60 years.
The mortality rate is 40% within the first month, and 50% of
patients who survive will require long-term special care.

Types:

Stroke is classified as resulting from two major mechanisms:

ischemia and hemorrhage.

Ischemic strokes, which account for 87% of all strokes, are

categorized by causes as thrombotic, embolic, or
hypoperfusion related.

Hemorrhagic strokes are subdivided into intracerebral

(accounting for 10% of all strokes) and nontraumatic
subarachnoid hemorrhage (accounting for 3% of all strokes)1

The final common pathway for all these mechanisms is

altered neuronal perfusion.

Neurons are exquisitely sensitive to changes in cerebral blood

flow and die within minutes of complete cessation of
perfusion. This fact underlies the current treatment emphasis
on rapid reperfusion strategies.

Transient ischemic attack (TIA) the standard definition of TIA

requires that all neurologic signs and symptoms resolve within
24 hours regardless of whether there is imaging evidence of
new permanent brain injury; stroke has occurred if the
neurologic signs and symptoms last for >24 hours.

A. Ischemic Stroke

Ischemic strokes, comprising thrombotic, embolic, and

lacunar occlusions, account for over 80% of all strokes
and result in cerebral ischemia or infarction.
A variety of disorders of blood, blood vessels, and heart
can cause occlusive strokes, but the most common by far
are atherosclerotic disease (especially of the carotid and
vertebrobasilar arteries) and cardiac abnormalities.

Essentials of Diagnosis

Secondary to thrombosis or embolism

Consider in acute neurologic deficit (focal or global) or

altered level of consciousness

No historical feature distinguishes ischemic from intracerebral

hemorrhagic stroke, although headache, nausea and
vomiting, and altered level of consciousness are more
common in intracerebral hemorrhagic stroke

Abrupt onset of hemiparesis, monoparesis, or quadriparesis;

dysarthria, ataxia, vertigo; monocular or binocular visual loss,
visual field deficits, diplopia
Pathophysiology

Acute occlusion of an intracranial vessel causes reduction in

blood flow to the brain region it supplies.

The magnitude of flow reduction is a function of collateral

blood flow and this depends on individual vascular anatomy,
the site of occlusion, and likely systemic blood pressure.

A decrease in cerebral blood flow to zero causes death of

brain tissue within 4-10 minutes;

If blood flow is restored prior to a significant amount of cell

death, the patient may experience only transient symptoms,
and the clinical syndrome is called a TIA.

Tissue surrounding the core region of infarction is ischemic but

reversibly dysfunctional and is referred to as the ischemic
penumbra. The penumbra may be imaged by using
perfusion-diffusion imaging with MRI or CT (see below and
Figs. 370-15 and 370-16). The ischemic penumbra will
eventually infarct if no change in flow occurs, and hence
saving the ischemic penumbra is the goal of
revascularization therapies.
Focal cerebral infarction occurs via two distinct pathways: (1) a
necrotic pathway in which cellular cytoskeletal breakdown is rapid,
due principally to energy failure of the cell; and (2) an apoptotic
pathway in which cells become programmed to die. Ischemia
produces necrosis by starving neurons of glucose and oxygen,
which in turn results in failure of mitochondria to produce ATP.
Without ATP, membrane ion pumps stop functioning and neurons
depolarize, allowing intracellular calcium to rise. Cellular
depolarization also causes glutamate release from synaptic
terminals; excess extracellular glutamate produces neurotoxicity by
activating postsynaptic glutamate receptors that increase
neuronal calcium influx. Free radicals are produced by membrane
lipid degradation and mitochondrial dysfunction. Free radicals
cause catalytic destruction of membranes and likely damage
other vital functions of cells. Lesser degrees of ischemia, as are
seen within the ischemic penumbra, favor apoptotic cellular death

causing cells to die days to weeks later. Fever dramatically worsens

brain injury during ischemia, as does hyperglycemia [glucose >11.1
mmol/L (200 mg/dL)], so it is reasonable to suppress fever and
prevent hyperglycemia as much as possible. Induced moderate
hypothermia to mitigate stroke is the subject of continuing clinical
research

48 EPISTAXIS

Definition

Epistaxis bleeding from the nose

Bleeding above the glottis (upper airway source)

Sensation of pooling of blood in the throat or need to

clear the throat before bleeding

Nasal blood supply

Origin 1: External Carotid artery

1. Facial artery Superior labial artery
Septum and nasal alae
2. Internal Maxillary artery
a. Sphenopalatine artery
Septum, middle and inferior turbinates
b. Pharyngeal artery
c. Inferior aspect of lateral nasal wall
d. Greater palatine artery
Anterior aspect of septum

Origin 2: Internal Carotid artery

1. Ophthalmic artery septum and lateral nasal walls
2. Anterior ethmoidal artery
3. Posterior ethmoidal artery

Sources of epistaxis:
1. Woodruff area

Inferior aspect of the lateral nasal wall, posterior to

the inferior turbinate (more posterior

Sphenopalatine + Pharyngeal arteries

Common source of severe nontraumatic bleeds

2. Kiesselbach plexus

Most common source of nose bleeds

Anteromedial aspect of the nares

Anterior ethmoidal + Greater palatine +

Sphenopalatine + Superior labial arteries

Etiology
LOCAL
Trauma
Anatomic deformities
e.g. Septal deflections, bony spurs,
fractures

*Anything obstructive can lead to

disruption of air flow resulting to turbulent
air flow anterior to the defect causing
draying effect, increasing opportunity for
mucosal disruption

Inflammatory reactions

Bacterial sinusitis, allergic rhinitis,

nasal polyposis, Wegner
granulomatosis, Tuberculosis,
Sarcoidosis

Intranasal tumors, vascular

malformations
e.g. Inverted papilloma,
angiofibroma, aneurysm,
encephalocele, hemangioma,
adenocarcinoma

Symptoms

Easy bruisability

Bleeding tendencies
Causes

Dry conditions created by heated indoor air during cold

season can dehydrate airways and predispose nasal
mucosa to cracking

Repeated blowing and wiping of nose, blunt trauma,

nose picking can abrade and injure mucosal surface
Physical examination

Examine hemodynamically stable patient in sitting

position to allow blood to exit anterior nose and minimize
ingestion or aspiration

Ask patient to clear each nostril of clots then pinch entire

cartilaginous portion of the nose for 15 minutes
continuously

Insert nasal speculum and examine both sides of the nose

for bleeding and the integrity of the septum

Observe the posterior oropharynx for 10 to 15 seconds to

confirm whether fresh blood is flowing down the back
wall which suggests a posterior source

Treatment
ANTERIOR EPISTAXIS

Minimally invasive and technically simple methods are

preferred

Gentle opiate or benzodiazepine sedation for vasoconstriction

and local anesthesia

1% phenylephrine

4% cocaine

2% lidocaine-epinephrine

Once bleed visualized Simple cautery with Silver Nitrate

Persistent bleeding Nasal packing with phenylephrine,

cocaine, or lidocaine-epinephrine Push superiorly until the
nostril is packed

Or use Nasal tampons

Give Amoxicillin-clavulanate BID for prophylaxis against

Bacterial sinusitis in patients with nasal pack

Packing material should be removed in 3 to 5 days

POSTERIOR EPISTAXIS

Foley catheter, nasal balloon device inflated to tamponade

bleeding site

If packing is needed admit for airway observation,

prophylactic antibiotics, ENT consultation

SYSTEMIC
Hypertension
Most common finding in
severe or refractory
epistaxis
Aberrations in clotting ability

Medications aspirin,
clopidogrel, NSAIDs, warfarin

Inherited bleeding diatheses

Hemophilia A (Factor VIII)
Hemophilia B (Factor IX)
Von Willebrand disease (vWF
is essential to Factor VIII
function)

Vascular/cardiovascular
diseases
Congestive heart failure
Arteriosclerosis
Collagen abnormalities

Clinical manifestations

Risk factors

Medications
1. Antiplatelets
2. Anticoagulants (e.g. Warfarin)

Renal failure

Hemophilia

Pregnancy

References
1.
2.

Bailey B. J. Head and Neck SurgeryOtolaryngology. 4th ed.

Philadelphia, PA: Lippincott Williams & Wilkins; 2006.
Current Diagnosis and Treatment: Emergency Medicine, 6th edition

50 APPENDICITIS
Definition
Inflammation of the vermiform appendix, ranging from a simple
catarrhal/congestive form to a more complicated transmural
involvement resulting to a perforated appendix
Anatomy
Vermiform Process or Appendix

A long, narrow, worm-shaped tube

With a small canal throughout its length that

communicates with the cecum by an orifice below and
behind the ileocecal opening, sometimes guarded by a
semilunar valve

Function: immunologic secretes Ig (IgA)

Location:

McBurneys point: 1/3 of the way up the line joining the

right anterior superior iliac spine to the umbilicus

Originates from the apex of the cecum

*Trace the taenia coli of the cecum to the base of the
apex where they converge to form the longitudinal
muscle coat

Held in position by the mesenteriole: fold of peritoneum

from the left leaf of the mesentery

Common positions of the tip of the appendix:

*1 and 2 most common
1. Hanging down in the pelvis, against right pelvic wall
2. Coiled up behind the cecum
3. Projecting upward along lateral side of cecum
4. In front of or behind terminal ileum

Size: < 1 cm to > 30 cm (ave. 6 9 cm)

Nerve supply

Superior mesenteric plexus:

1. Parasympathetic
2. Sympathetic afferent (sensory fibers):
conduct visceral pain from the appendix, enter
spinal cord at T10

Blood supply: Appendicular artery

Located between the 2 folds of the mesenteriole, close to

the free margin

Origin: Ileocolic artery, from Superior mesenteric a.

Venous drainage: Appendicular vein

Drains to Ileocolic vein, tributary of Superior mesenteric v.

Lymph drainage: one or two intermediate nodes in the

mesoappendix, drain to Superior mesenteric LNs
Histology
1. Serous

Complete except along the line of attachment of the

mesenteriole
2. Muscular

Longitudinal muscle fibers

Does not form 3 bands unlike rest of large intestine

Complete except at one or two points that allow

contiguity of peritoneal and submucous coats

Circular muscle fibers thicker layer

3. Submucous

Contains large number of masses of lymphoid tissue

which may cause mucous membrane to bulge into the
lumen and decrease its size
4. Mucous

Columnar epithelium

Fewer intestinal glands compared to rest of large intestine

Etiology

Dominant etiologic factor obstruction of the lumen

Most common cause of obstruction Fecaliths: accumulation

and inspissation of fecal matter around vegetable fibers

Other causes of obstruction:

Hypertrophy of lymphoid tissue (Viral, e.g. measles)

Inspissated barium from previous X-ray studies

Tumors

Vegetable and fruit seeds

Intestinal parasites (e.g. Pinworms, Ascaris, Taenia)

Other etiologic factors:

Infection with Yersinia: high complement fixation

Pathogenesis
LUMINAL OBSTRUCTION
Continuing normal mucosal
secretion (capacity: 0.1 mL)
RAPID DISTENTION
Stimulation of visceral
afferent stretch fibers

Peristalsis

Vague, dull, diffuse pain

in the mid-abdomen or
lower epigastrium

Cramping
Continued rapid mucosal
secretion and multiplication of
resident bacteria

INCREASED DISTENTION
Severe visceral pain

Nausea and vomiting

Increased luminal pressure

Venous pressure exceeded

Continuous arterial inflow

Capillaries and veins occluded

ENGORGEMENT AND CONGESTION
Infarction

Increased bacterial
invasion
PERFORATION

Inflammation of
parietal peritoneum
Shift of pain to RLQ

Stages of Appendicitis
1. UNCOMPLICATED

Congestive or Catarrhal due to mucosal and

submucosal inflammation only

Suppurative the whole appendix becomes swollen,

turgid, and loses its healthy sheen and is coated with a
fibrinous exudate
2. COMPLICATED

Gangrenous due to unrelieved obstruction, the capillary

pressure is overcome, which will lead to decreased blood
flow with vessel thrombosis and full thickness necrosis

Perforative if gangrenous appendicitis is not treated,

then perforation may ensue and take one of the following
two events:

Outporuring of inflammatory cells and mediators

from parietal peritoneum and serosa of adjacent
visceral structures may confine the perforation and
eventually lead to a walling off effect leading to a
formation of periappendicial abscess

Failure of the above mechanism may lead to

perforated appendix, with spillage of contaminated
appendiceal content leading to spreading peritonitis,
which may be localized or generalized
*Perforation is not common if symptoms have been
present in less than 24 hours
Bacteriology

Principal organisms seen in the normal appendix, acute

appendicitis, and perforated appendicitis:

Escherichia coli

Bacteroides fragilis

Other common organisms in acute appendicitis

AEROBIC and FACULTATIVE
ANAEROBIC
Gram-negative bacilli
Gram-negative bacilli
Escherichia coli
Bacteroides fragilis
Pseudomonas aeruginosa
Other Bacteroides species
Klebsiella species
Fusobacterium species
Gram-positive cocci
Gram-positive cocci
Streptococcus anginosus
Peptococcus species
Other Streptococcus species Gram-positive bacilli
Enterococcus species
Clostridium species

NOTE: appendicitis is a polymicrobial infection, and often the

flora is known. Therefore, routine culture of intraperitoneal
samples is questionable.

Peritoneal culture is reserved for:

1. Immunosuppressed due to illness or medication
2. Abscess formation after treatment of appendicitis

Clinical Manifestations
SYMPTOMS
ANOREXIA ABDOMINAL PAIN VOMITING

Abdominal pain prime symptom

Initially diffusely centered in the lower epigastrium or

umbilical area, moderately severe, steady, sometimes
superimposed with intermittent cramping
*Corresponds to the visceral afferent innervation: T10 level

After 1 to 12 hours (but usually within 4 to 6 hours), pain

localizes to the right lower quadrant
*Corresponds to the somatic innervation triggered by the
pain in the area of the appendix

HOWEVER, variations in anatomic location of appendix

account for variations in the principal locus of pain
1. May begin at the left lower quadrant and stay there
2. Retrocecal appendix flank or back pain
3. Pelvic appendix suprapubic pain
4. Retroileal appendix testicular pain (due to irritation
of spermatic artery and ureter)

Anorexia almost always accompanies appendicitis

Vomiting in 75% of patients, neither prominent nor prolonged

Due to neural stimulation and ileus

Change in bowel movement varies:

Obstipation: beginning before onset of abdominal pain

Diarrhea may occur especially in children

SIGNS

Patient prefers to lie supine, with thighsparticularly the right

drawn up, because motion increases pain

Right lower quadrant signs: due to localized peritoneal

irritation caused by the inflamed appendix

CARDINAL SIGN: localized tenderness maximal at/near

McBurney point

Direct rebound tenderness

Referred or indirect rebound tenderness

Cutaneous hyperesthesia in areas supplied by spinal nerves on

the right at T10, T11, T12

May be the first positive sign in many cases

Elicited by needle prick or gently picking up skin between

forefinger and thumb

Muscle resistance to palpation of the abdominal wall

Parallels severity of inflammation

Begins as voluntary guarding and increasingly becomes

involuntary muscle spasms

Pelvic appendix pararectal tenderness on DRE

ROVSING SIGN pain at RLQ when palpatory pressure is

exerted in the left lower quadrant

ILIOPSOAS SIGN patient lies on the left side while examiner

extends patients right thigh (stretch iliopsoas) Pain

OBTURATOR SIGN passive internal rotation of flexed right

thigh while patient is supine Pain

DUNPHY SIGN sharp pain in RLQ elicited by voluntary cough

MARKLE SIGN pain elicited in a certain area of the abdomen

when the standing patient drops from standing on toes to the
heels with a jarring landing

Vital signs are minimally changed

Temperature elevation is rarely > 1C

Pulse rate is normal or slightly elevated

GREATER CHANGES = possible complication

Signs of mild to moderate dehydration

Thirst

Few or no tears when crying

Xerostomia

Headache

Dry skin

Constipation

Decreased urine output

Dizziness or lightheadedness

Sleepiness or tiredness
Pelvic appendix requires rectal exam

Pain elicited in suprapubic area and within rectum

Diagnosis
ROUTINE LABORATORY WORK-UP
1. Complete Blood Count

Mild leukocytosis (10,000 18,000 cells mm3) with

moderate polymorphonuclear predominance

If > 18,000 cells/mm3 consider perforated appendix

2. Urinalysis

Rule out:

Urinary tract infection

Ureteral stone
NOTE: presence of these entities does not completely
rule out appendicitis

Bacteriuria usually not seen

3. Serum HCG

Done in women of child-bearing age if there is a

possibility of pregnancy
IMAGING STUDIES

Graded compression sonography

Appendix: blind-ending, non-peristaltic bowel loop

originating from the cecum

Diameter measured in the AP dimension

NORMAL APPENDIX
APPENDICITIS
Easily compressible
Non-compressible
5 mm AP diameter 6 mm AP diameter
(+) Appendicolith
Thickening of appendiceal wall
(+) Periappendiceal fluid

For women, be sure to perform trans-abdominal or

endovaginal UTZ to rule out gynecologic pathology

Sensitivity: 55 96%; Specificity: 85 98%

High resolution helical CT-scan: superior to ultrasound

Findings for appendicitis:

1. Dilated appendix (> 5 cm), thickened wall
2. Dirty fat
3. Thickened mesoappendix
4. (+) Phlegmon
5. Arrowhead sign: thickening of cecum causes
funneling of agent towards orifice of appendix

Sensitivity: 80 97%; Specificity: 93 94%

ALVARADO SCALE FOR THE DIAGNOSIS OF APPENDICITIS

1. Scale
MANIFESTATIONS
VALUE
Migration of pain
1
Symptoms
Anorexia
1
Nausea and/or vomiting
1
Right lower quadrant tenderness
2
Signs
Rebound tenderness
1
Elevated temperature
1
Leukocytosis
2
Laboratory values
Left shift in leukocyte count
1
Total points
10
2. Interpretation
SCORE
INTERPRETATION
ACTION
Further work-up of little value
9 10
Certain
Proceed to OR
78
High likelihood
CT scanning is appropriate
Compatible but not
56
diagnostic
Extremely unlikely
04
CT scanning is not justified
(but not impossible)

Laparoscopy

Diagnostic and therapeutic for acute abdominal pain

Most useful for females with lower abdominal complaints,

to differentiate gynecologic pathology from appendicitis

Clinical algorithm for suspected cases of acute appendicitis

History and physical examination

Classic appendicitis:
Short duration of pain
Abdominal rigidity
Migration of pain to RLQ
Equivocal presentation
Pain centered in RLQ
RLQ tenderness
Anorexia

Male or non-pregnant
female

CT-scan

Pregnant

UTZ

Appendicitis

Indeterminate
results

Appendectomy

UTZ

d.

3.

Antibiotic treatment alone may delay diagnosis

of significant pathology such as carcinoid or
carcinoma
CONCLUSION: no laboratory test or clinical
investigation can reliably distinguish patients whose
appendicitis is amenable to conservative treatment;
therefore, surgery still remains the gold standard

NON-PHARMACOLOGIC
Open Appendectomy
1. Before incision, perform PE of the abdomen to detect any
mass and determine site of incision
2. Incision

McBurney/Gridiron incision

Oblique incision in the RLQ over McBurneys point

Rocky-Davis incision

Transverse incision in the RLQ over McBurneys point

Battle pararectal/Vertical incision

Rarely performed because of tendency for

dehiscence and herniation

Normal or
alternative
diagnosis

Supportive care
or treatment

Management
APPENDICEAL RUPTURE

Rate of perforated appendicitis: 25.8%

Most common in:

Children < 5 years old

Adults > 65 years old

Most frequent location:

Distal to the point of luminal obstruction, along antimesenteric border of the appendix

Clinical manifestations:

Fever of > 39C

WBC count > 18,000 cells/mm3

Antibiotic prophylaxis for prevention of postoperative wound

infection (most common postoperative complication of
appendicitis)

Non-perforated appendicitis: no benefit in extending

coverage beyond 24 hours

Perforated appendicitis: 7 10 days therapy, continued

until patient is afebrile and WBC is normal

NOTE: give IV antibiotics until WBC count is normal and

patient is afebrile for 24 hours
PHARMACOLOGIC

Crystalloids correct any existing fluid and electrolytes deficit

Pain medication start when dx of appendicitis is secured

Antibiotics

Second generation Cephalosporin

UNCOMPLICATED

Cefoxitin, Cefotetan, Cefuroxime

Just before or at the time of surgery

Broad spectrum antibiotic with aerobic

COMPLICATED
and anaerobic coverage

ANTIBIOTICS AS DEFINITIVE THERAPY

RCT involving 252 men18 50 years old

1. Antibiotics alone may be reasonable therapy for
acute appendicitis
2. Issues:
a. Limited applicability due to limited patient pool
b. Perforation was 9% in antibiotic group
compared to 5% for those operated on
c. Follow0up was only 1 year

3.

4.

5.

6.

Exposure of the appendix

Dissection of abdominal wall fascia (Scarpas fascia) and

underlying muscular layers to gain access to peritoneum

Peritoneum is opened transversely and entered

Note character of any peritoneal fluid to help

confirm diagnosis. Suction from the field, if purulent
collect and culture.

Place retractors into peritoneum

Identify cecum and retract medially

Exteriorize cecum using a moist gauze sponge or

Babcock clamp, follow taeniae coli to base of appendix
beneath the ileocecal valve (Bauhin valve)

If appendix appears normal, other causes for the

condition should be sought:

Ovarian pathology

Meckels diverticulum

Sigmoid disease
Removal of appendix

Hold mesoappendix between clamps, divide, ligate.

Clamp appendix proximally about 5 mm above the

cecum to avoid contamination of peritoneal cavity.

Cut with scalpel above the clamp.

Ligate appendix to prevent bleeding and leakage.

Cauterize residual mucosa of the appendix to avoid

mucocele.
Placement of the cecum

Use purse-string suture or z-stitch to invert cecum

Place cecum back in the abdomen

Closure

Irrigate abdomen

If perforation occurred, perform peritoneal lavage with

several liters of warm saline. Aspirate all irrigation fluid to
avoid spreading of infection.

Close peritoneum with running suture

Reapproximate and close fibers of muscular and fascial

layers with continuous or interrupted absorbable suture

Close skin with subcutaneous sutures or staples

Laparoscopic Appendectomy

Use of three trocar insertion sites:

1: Umbilicus

2: Suprapubic position

3: variable, depending on location of the appendix and

surgeon preference LLQ, epigastrium, or RUQ
Effective management of acute appendicitis but
undetermined comparability to open appendectomy
Of little benefit in comparison to open appendectomy

Advantages:
1. Beneficial in obese patients due to difficulty of
gaining adequate access through small RLQ incision
2. Shorter hospital length of stay
3. Shorter period before return to normal activity
4. 50% less wound infections after procedure compared
to open appendectomy

Disadvantages:
1. Higher cost and duration of surgery
2. Three times more likely to develop intra-abdominal
abscess compared to open appendectomy

Natural Orifice Transluminal Endoscopic Surgery (NOTES)

Use of flexible endoscopes inserted through natural, alreadyexisting external orifices, to gain access into abdominal cavity

Transvaginal removal of appendix has been performed

Possible advantages reduced postoperative wound pain,

shorter convalescence, avoidance of wound infection and
abdominal-wall hernias, absence of scars
FOLLOW-UP
UNCOMPLICATED

COMPLICATED

Return 5 7 days after surgery for removal

of wound stitches
Case to case basis
Consider wound healing, use of drain,
antibiotic coverage

PROGNOSIS

Morbidity

Early post-operative problems:

1. Ileus
2. Surgical site infection
3. Intraabdominal abscess
4. Fecal fistula

Delayed post-operative problems:

1. Intestinal obstruction secondary to adhesions
2. Incisional hernia

Mortality

Rate:
1. Non-perforated 0.6%
2. Ruptured 3.0%
*Increased to 50% in elderly

Predictors:
1. Age
2. Rupture

Causes of mortality: sepsis following untreated,

1. Peritonitis
2. Intraabdominal abscess
References
1. Acute Appendicitis by Dr. Alberto P. Paulino Jr., Handbook of
Medical and Surgical Emergencies, 6th edition
2. Schwartzs Principles of Surgery, 9th edition