1 ABC of Basic Life Support (AHA, 2010 Guidelines)

Basic Life Support is the foundation for saving lives following sudden
cardiac arrest which, despite progressive advances in prevention,
continues to be a leading cause of death in many parts of the world.
Sudden cardiac death has many etiologies, cardiac or non-cardiac, can
occur in a variety of circumstances, witnessed or unwitnessed, and
different settings, out-of-hospital, or in-hospital. Thus a universal strategy for
successful resuscitation is needed. The actions comprising this strategy are
called the links in the Chain of Survival which include:

(1) Immediate recognition of cardiac arrest and activation of

the emergency response system
1. An adult is found unresponsive or witnessed to suddenly
collapse. Ensure that the scene is safe.
2. Check for response by tapping on the shoulder and shouting,
Hey, hey, are you okay? x2 No response
3. Activate the EMS and somebody get me an AED!
(2) Early cardiopulmonary resuscitation
Formerly sequenced as Airway-Breathing-Circulation or ABC, a
change in the previous American Heart Association Guidelines
recommends the initiation of chest compressions before
ventilations thus the new sequence is CAB.
1. Extend the head to expose the neck. Take 10 seconds to feel
for the pulse. No pulse
2. Start chest compressions forceful rhythmic applications of
pressure which create blood flow by increasing intrathoracic
pressure and directly compressing the heart which then
generates blood flow and oxygen delivery to the
myocardium and brain.
Place the heel of one hand over the heel of the other
hand on the sternal notch, position the shoulders over
hands with elbows locked and arms straight
Push hard and push fast: 100 compressions/minute with a
depth of at least 2 inches or 5 cm
Allow complete recoil of the chest after each compression
to allow the heart to fill completely
3. Start rescue breaths by mouth-to-mouth or bag-mask to
provide oxygenation and ventilation.
Open airway by performing head tilt/chin lift maneuver or
jaw thrust for suspected victims of cervical spine injury
Deliver each rescue breath over a full second, ensure it is
sufficient to produce visible chest rise
Use a compression to ventilation ratio of 30 chest
compressions to 2 ventilations for 5 cycles
*IF an advanced airway (Endotracheal tube, LMA) is in
place, give 1 breath every 6 to 8 seconds and there should
be no pause in compressions or ventilations
(3) Rapid defibrillation (Vtach/Vfib) attach the AED, turn it on,
follow the prompts, resume chest compressions after shock
(4) Effective advanced life support
(5) Integrated post-cardiac arrest care

During Cardiopulmonary resuscitation check for:

1. Hypovolemia
2. Hypoxia
3. Hydrogen ion (Acidosis)
4. Hypo/hyperkalemia
5. Hypoglycemia
6. Hypothermia
7. Toxins
8. Tamponade (Cardiac)
9. Tension pneumothorax
10. Thrombosis (Coronary or Pulmonary)
11. Trauma

2 UPPER AIRWAY OBSTRUCTION

Acute upper airway obstruction is a sudden blockage of the
upper airway, anywhere from the anterior nares to the distal end
of the trachea, that interrupts normal breathing.
In the presence of a fixed obstruction in the upper airway,
forced inspiration creates a large negative intrathoracic pressure
below the level of the obstruction with a subsequent narrowing
of the extrathoracic trachea, resulting in increased turbulence
and velocity of airflow which causes the vocal cords and
aryepiglottic folds to vibrate thus causing a harsh vibratory sound
of variable pitch termed stridor. Obstruction is greater during
inspiration than expiration.
In children, the most common causes of upper airway
obstruction are infections or anatomic abnormalities. In general,
these etiologies share the following clinical manifestations:
inspiratory stridor, brassy cough (seal bark), and difficulty
breathing.
ACUTE INFECTIOUS CAUSES

ACUTE NON-INFECTIOUS CAUSES

FOREIGN BODY
ASPIRATION
Large foreign body
lodges in the larynx,
trachea, or bronchus
causing obstruction
Choking, gagging
Wheeze

BACTERIAL
TRACHEITIS

Acute
bacterial
infection of
the upper
respiratory
tract

GA Strep
Anaerobes
S. aureus

EPIGLOTTITIS

Infection of
the epiglottis
and
aryepiglottic
folds and
surrounding
soft tissue

S. aureus
Hib

LARYNGOTRACHEOBRONCHITIS
Airway swelling in
the supraglottic
and glottic area
usually secondary
to a viral cause

Hib
GB Strep
S. pneumoniae
S. aureus

High fever
Respiratory
distress
Neck stiffness
Bulging neck
mass
Gurgling
respiration

RETROPHARYNGEAL
ABSCESS
Infection of the
potential space
between the
posterior
pharyngeal wall
and prevertebral
fascia

Fulminant
Respiratory
distress
Sniffing
position

Parainfluenza 1,3
RSV, Influenza,
Adenovirus

Coryza

CBC, X-ray:
Swollen
epiglottis
(Thumb Sign)

CBC, Xray:
Ragged
irregular
tracheal
border
Cefotaxime,
Ceftriaxone,
AmpicillinSulbactam
CBC, X-ray:
Thickened
retropharyngeal
space

X-ray: Subglottic
narrowing
(Steeple Sign)

Intubation
Cefotaxime,
Ceftriaxone,
Ampi-Sul
Antibiotics
Surgical
drainage

Mist vaporizer
Racemic
Epinephrine
Dexamethasone

X-ray
Bronchoscopy:
Diagnostic and
therapeutic
Infants: 5 interscapular
back blows with childs
head lower than chest
alternating with five
chest compressions
Older: Heimlich
maneuver

ANGIOEDEMA

SPASMODIC CROUP

Acute laryngeal
swelling causing
obstruction

Airway swelling in the

supraglottic and glottic
area secondary to a
non-infectious cause
(allergic, psychologic)
Coryza

Anaphylactic
shock:
Pruritus
Urticaria
Swelling of the
lips, tongue
X-ray: subglottic
narrowing

Epinephrine
IVF
Steroids

X-ray: Subglottic
narrowing

Cool mist

CHRONIC
CAUSES

PERITONSILLAR
ABSCESS

Infection of the
potential
space
between the
superior
constrictor and
tonsils

GA Strep
Anaerobes

Severe throat
pain
Trismus
Torticollis
Hot potato
voice
CBC
Endoscopy

Antibiotics
Surgical
drainage

CHOANAL
ATRESIA
Persistence of
the buconasal
membraine in
the posterior
margin of hard
palate
Most common
congenital
anomaly of
nose
Unilateral:
Mucoid
rhinorrhea,
sinusitis
Bilateral:
Apnea,
cyanosis, RD
Inability to pass
nasal catheter
High resolution
CT scan
Surgery

LARYNGOMALACIA/
TRACHEOMALACIA
Laryngomalacia defect or
delayed maturation of
supporting structures of larynx
causing prolapse of epiglottis,
arytenoids, aryepiglottic folds
Tracheomalacia inadequate
cartilaginous and myoelastic
elements supporting trachea
leading to abnormal tracheal
collapse
Worsens with crying, exertion,
feeding
Improves with prone position or
neck extension

VASCULAR
ANOMALIES
Variation in
normal vascular
anatomy
causing
obstruction of
the trachea or
bronchus

Endoscopy: Flabby supraglottic

structures/anterior collapse of
trachea

Endoscopy
CT scan

Reassurance and respiratory

support
Resolves spontaneously by 24
months, if not:
Tracheobronchomalacia
requiring surgery

Surgery

Worsens with
feeding
Improves with
neck extension

TRACHEOSTOMY

Indications:
1. Congenital abnormality of the larynx or trachea
2. Long term unconsciousness or coma
3. Relieve upper airway obstruction
4. Improve respiratory function
5. Respiratory paralysis
6. Emergency: failed intubation
Technique
1. Find the indentation between the thyroid cartilage and
cricoid cartilage which marks the area of the cricothyroid
membrane.
2. Make a half inch horizontal incision about an inch deep.
3. Pinch the incision or insert a finger inside the slit to open it.
4. Insert the tracheostomy tube into the incision half an inch to
one inch deep.
5. Deliver two quick breaths. Pause for 5 seconds. Then give a
breath every 5 seconds.

3 ACUTE ASTHMA EXACERBATION

Asthma is a chronic inflammatory condition of the airways
resulting in episodic airflow obstruction secondary to hyperresponsiveness to provocative exposures or triggers.
Acute asthma exacerbation is an acute or subacute episode of
decompensated asthma characterized by progressively
worsening shortness of breath, cough, wheeze, and chest
tightness, or a combination of all these symptoms.
Asthma exacerbation can be triggered by IgE-mediated factors
such as dust mites, pollens, and animal dander; non-IgEmediated factors such as irritants, cold air, noxious fumes, viral
infections, and physical exertion; and gastroesophageal reflux. It
may also be due to an underassessed, or under treated asthma.
Exposure or the presence of these triggers leads to an
immunologic hyper-responsiveness. In the early phase, within 15
to 30 minutes of exposure, bronchoconstriction is the
predominating factor leading to airway obstruction. In the late
phase, 4 to 12 hours after allergen exposure, tissue inflammation,
immune cellular infiltration into the airways, airway edema, and
excess mucus production exacerbate airway obstruction. The
resulting airway obstruction then leads to nonuniform ventilation
such that ventilation/perfusion mismatch occurs resulting to
alveolar hypoventilation with a concomitant increased in arterial
Carbon dioxide partial pressure and decrease in arterial Oxygen
partial pressure. Airway obstruction also predisposes to
hyperinflation such that there is a decrease in compliance
resulting to an increase in work of breathing which also
exacerbates the hypoxemia. The hypercarbia and hypoxemia
and
concomitant
acidosis
stimulates
pulmonary
vasoconstriction, and with inadequate perfusion a decrease in
surfactant production occurs increasing the risk for atelectasis.
In general, asthma exacerbations are heralded by the presence
of tight, non-productive cough, that is accompanied by other
symptoms and signs that mark the severity of the case either as
mild, moderate, or severe. It is important to determine the
severity of exacerbation in order to guide treatment decisions.
Breathlessness, positional preference, level of consciousness,
respiratory rate, retractions, wheezing, pulse rate, pulsus
paradoxus, nighttime awakenings, limitation in activity, are
parameters used to determine the severity of exacerbation and
even to identify whether there is risk for impending respiratory
arrest. The frequency of these manifestations also give
information on the severity of the exacerbation. In the
emergency room, practical measures that can be taken in order
to determine the level of asthma severity include pulse oximetry
which shows the level of oxygen saturation. For those who are
not known cases of asthma, a Salbutamol Challenge test can be
performed in order to demonstrate whether the airway
obstruction is responsive to a bronchodilator, which is suggestive
of asthma.

Other laboratory and ancillary procedures may also be

requested if there is an indication to do so. A Chest X-ray may be
requested to screen for potential complications such as
pneumothorax. Further pulmonary function tests can also be
requested in order to assess for the degree of airway obstruction
which gives an idea on the long-term course of the
exacerbation as well as the level of control achieved by the
existing treatment. Such tests include Spirometry or peak flow
meter to measure FEV1 or Peak Expiratory Flow Rate. However,
these tests are impractical in the setting of a patient in acute
exacerbation who is in respiratory distress. In patients who are
not responding to initial management and have a progressively
worsening course arterial blood gas determination is important
to determine the need for ventilation and to guide the manner
in which ventilation will be given.
Again, management should be guided by the level of severity of
the exacerbation. For all patients, oxygen should be given if
oxygen saturation is below 90%. In patients with mild to
moderate exacerbation an inhaled short acting beta 2 agonist
such as Salbutamol should be given every 20 minutes for 1 hour.
This is followed by an oral systemic corticosteroid such as
prednisone. In patients with severe exacerbation high dose
inhaled short acting beta 2 agonist with an anti-cholinergic such
as Ipratropium should be given every 20 minutes for 1 hour along
with the oral systemic corticosteroid. After the first hour of
management the patient should be reassessed. If the patient
continues to be in the same level of exacerbation the initial
treatment is sustained for another 3 hours. At the end of this
period if the patient shows good response to treatment by
manifesting with resolution of symptoms even 1 hour after the last
dose of medications, the patient may be discharged with the
appropriate instructions for maintenance medication which
should include an inhaled short acting beta 2 agonist and an
oral systemic steroid. If the patient shows incomplete response
hospital admission should be advised and the patient should be
maintained on the ongoing treatment until resolution. If the
patient shows poor response with progressive deterioration of
mental status admission to the intensive care unit should be
advised and preparations for possible intubation and
mechanical ventilation should be started. If in the onset, the
patient does not show any significant response to inhaled beta 2
agonist treatment and has no improvement after injection with
epinephrine, the patient may be considered as a case of Status
Asthmaticus or Acute Severe Asthma, at which point admission
to the intensive care unit with the same aforementioned
instructions should be advised.

4 PERINATAL ASPHYXIA
Perinatal asphyxia is the interference in the gas exchange
between the organ systems of the mother and the fetus resulting
to an increase in the arterial Carbon dioxide partial pressure with
a concomitant decrease in arterial Oxygen partial pressure as
well as a fall in pH.
The resulting energy deficit due to the hypercarbia and
hypoxemia in perinatal asphyxia shift the normal aerobic
metabolism to anaerobic metabolism thus leading to lactic
acidosis. The aberrancies in ventilation and pH levels then trigger
redistribution of blood towards the vital organs of the fetus which
are the brain, heart, and adrenal glands which results in a
subsequent hypoperfusion in the lungs, gastrointestinal tract, and
kidneys. However, as perinatal asphyxia progresses without
adequate intervention, oxygen debt in the brain builds leading
to an alteration in brain water distribution as well as predisposing
to multifocal brain ischemia. The resulting cytotoxic and
vasogenic edema contribute to brain swelling, which together
with the ischemia leads to further deterioration.
Perinatal asphyxia may be a consequence of complications
during labor and delivery such as interruption of umbilical blood
flow as in cord compression, failure of gas exchange across the
placenta as in placental abruption, inadequate perfusion of the
maternal side of the placenta as in maternal hypotension, the
presence of a compromised fetus that cannot tolerate the rigors
of normal labor characterized by intermittent transient hypoxic
episodes, as in those with anemia or intrauterine growth
retardation, and lastly, failure of the fetus to undergo the
necessary respiratory changes for survival outside the uterus,
namely expansion of the lungs at delivery.
According to the World Health Organization, 40% of under 5 year
old deaths occur during the neonatal period, 9% of which can
be attributed to perinatal asphyxia. The incidence is higher in
resource poor countries such as the Philippines where it occurs in
5 to 10 out of a 1000 live births. These statistics only emphasize
the need for every clinician to be familiar with the clinical
manifestations of perinatal asphyxia and the necessary steps for
successful resuscitation.
Perinatal asphyxia may be diagnosed based on the following
criteria: fetal acidosis reflected by pH of less than 7 or base
excess of more than12 mmol/l, APGAR score of 0 to 3 at 5
minutes, seizures, and multisystem organ failure.
The American Association of Pediatrics, together with the
American Heart Association, has provided a systematic step by
step algorithm for neonatal resuscitation in the presence of
perinatal asphyxia which is divided into 3 phases. Each phase is
conducted within 30 seconds to ensure prompt delivery of
resuscitation.
The first phase begins by evaluating four things: First, was the
neonate delivered at term gestation? Because more

complications are associated with preterm delivery, such as

respiratory distress syndrome. Second, was the amniotic fluid
clear? Because a meconium stained amniotic is suggestive of
asphyxia. Third, was the neonate crying or breathing at
delivery?. And fourth, did the neonate display good muscle
tone? If the answers to these four questions for initial assessment
are a yes: the neonate is at term, the amniotic fluid is clear, the
neonate was crying or breathing, and the neonate displayed
good muscle tone then routine neonatal care is given which is
comprised of first, providing adequate warmth. It is important to
ensure thermoregulation in neonates because they have a large
surface area to mass ratio and are prone to evaporative heat
loss thus are at high risk for hypothermia which leads to
complications such as hypoglycemia and increased work of
breathing. Warmth can be given by drying the neonate with
warm blankets, placing them in a radiant heat source, or
wrapping them in thermoregulatory plastic when indicated, as in
the case of very low birth weight neonates, those with a birth
weight of less than 1,500 g who are at an even higher risk of
hypothermia. Second, the neonate should be stimulated. In
vigorous infants that display good muscle tone and respiratory
effort, drying is enough to stimulate increase in heart rate and
breathing. Third, the airways should be cleared. This is done by
placing the neonate in a sniffing position which hypertextends
the neck so that the posterior pharynx, larynx, and trachea are
aligned to promote unimpeded air entry. Then, nasal and oral
suctioning are performed using a bulb syringe or suction
catheter. Lastly, the color of the neonate is checked. If the infant
is pink or acrocyanotic, the color is normal. But if central cyanosis
is present then further management is warranted.
In contrast, if the neonate was born pre-term, meconium
stained, was apneic or displayed poor respiratory effort, and had
poor muscle tone modifications in routine neonatal care are
warranted. In these neonates further stimulation is done by
flicking the soles or vigorously rubbing the trunk. Meconium
stained non-vigorous infants require tracheal suctioning as such,
may require endotracheal intubation.
If after the first 30 seconds or the first phase of management the
neonate continues to be apneic, bradycardic with a heart rate
of less than 100 bpm, or has persistent central cyanosis the
second phase is initiated with continuous supplemental oxygen
delivery at a rate of 5 LPM at 100% via face mask or flow inflating
bag mask. If after 15 seconds of oxygen supplementation no
improvement occurs, positive pressure ventilation is started at 40
cm H20, 100% using a cushioned mask with a flow inflating bag
or T-piece connector. Bag mask ventilation is given at a rate of
40 to 60 breaths per minute. If after another 15 seconds however,
the heart rate is still below 60 bpm, the third phase is initiated
with chest compressions delivered at the lower 1/3 of the
sternum, at a depth of 1/3 the AP diameter of the chest, at a

rate of 3 compressions to 1 ventilation every 2 seconds using

either the two finger technique wherein the third and fourth
digits of the same hand perform compressions while the other
hand supports the back of the neonate, or the two thumb
circling hand technique wherein both hands encircle the
neonate with the thumbs delivering the compressions. The
second technique has been shown to increase peak systolic and
coronary perfusion pressure more effectively than the first. If after
30 seconds the heart rate continues to be less than 60 bpm
Epinephrine may be given at an IV dose of 0.1 to 0.3 ml/kg every
3 to 5 minutes. Or if an IV line has not been instituted, an NGT
dose of 0.3 to 1 ml/kg can be given until access has been
established. If no improvement is noted after another 30 seconds
other causes for asphyxia must be entertained. First,
hypovolemia should be ruled out. If the neonate displays pallor,
weak pulses, and delayed capillary refill time, IV PNSS should be
started at 10 ml/kg over 5 to 10 minutes. If improvement still does
not occur it is important to rule out any congenital cardiac
abnormalities, airway malformations, pneumothorax, or
diaphragmatic hernia. In the setting of pneumothorax, needle
aspiration using a 20 gauge needle inserted at the 4th ICS AAL or
2nd ICS MCL should be performed. In the case of diaphragmatic
hernia stomach decompression should be performed via a
gastric tube and intubation should be instituted immediately.

6 ANAPHYLAXIS AND ANAPHYLACTOID REACTIONS

Anaphylaxis is an IgE mediated, antigen induced reaction
causing the massive release of biochemical mediators from
previously sensitized mast cells and basophils leading to a clinical
syndrome characterized cutaneous, respiratory, cardiovascular,
and gastrointestinal tract manifestations. In comparison, an
anaphylactoid reaction is a non-IgE mediated reaction involving
complement activation, direct mast cell activation, and/or
arachidonic acid metabolism alteration by intake of
acetylsalicylic acid or nonsteroidal anti-inflammatory drugs
resulting to manifestations similar to that of anaphylaxis.
Anaphylaxis or anaphylactoid reactions can be a consequence
of exposure to sensitizing agents such as allergens,
pharmacologic agents, exercise, and in rare cases idiopathic.
Symptoms usually begin within moments of exposure to
causative agents. Early changes include sneezing, pruritus,
hoarseness, the feeling of a lump in the throat and may rapidly
progress to diaphoresis, difficulty of breathing, disorientation, and
loss of consciousness.
Diagnosis in the emergency setting is achieved clinically
because locally, no specific diagnostic test can adequately
determine anaphylaxis. In the United States assay of Tryptase, a
mast cell derived preformed mediator, has been used to
document massive mast cell activation. Once the patient is
stable, hypersensitivity skin tests, IgE tests, or challenge tests can
be performed to identify the specific causes of anaphylaxis.
When a patient presents with anaphylaxis in the emergency
setting the main goal of management is to block the action of
histamines
on
peripheral
tissues.
IM
Epinephrine,
Diphenhydramine, or Histamine Receptor blockers may be used
for this purpose. Late anaphylaxis may be prevented by
administering IV corticosteroids such as Methylprednisolone or
Hydrocortisone or giving oral Prednisone if the patient is stable. In
patients suffering from hypotension rapid IV infusion with NSS at 5
to 10 ml/kg as bolus during the 1st 5 minutes of treatment should
be given. Epinephrine infusion can also be started and if
ineffective, Dopamine should be given. In patients with upper
airway obstruction a Beta 2 agonist can be started as
nebulization, and if intractable to both Epinephrine and Beta 2
agonists, endotracheal intubation or even tracheostomy may be
indicated. In patients taking Beta blockers for hypertension,
Calcium channel blockers should be substituted in order to
prevent exacerbation of the ongoing Beta blockade. IV
Glucagon and Atropine can also be used to reverse Beta
blockade. Patients should be monitored for at least 24 hours for
late anaphylaxis. Discharge medications should include oral
Antihistamines with or without oral Prednisone for 3 to 5 days.

8 DIARRHEAL DISEASES AND DEHYDRATION

Diarrhea is the passage of 3 or more liquid stools in a 24 hour
period resulting to an excessive loss of fluid and electrolyte in the
stools. It may be acute or chronic, lasting for 2 weeks or longer.
Diarrhea is considered an emergency because of the
complications attributed to the concomitant dehydration in
these cases. Dehydration is contraction of the extracellular
volume in relation to cellular mass that may result from external
loss of water and salt, or salt alone, or water alone.
The most common cause of acute diarrhea in any age group is
gastroenteritis, other possible causes include systemic infections,
and as a side effect of intake of antibiotics. The mechanisms for
diarrhea include Secretory diarrhea in which a secretagogue
binds to bowel epithelium resulting to intracellular accumulation
of cAMP leading to excessive secretion and decreased
absorption such that diarrhea persists even with fasting. An
example is Cholera. Another mechanism is Osmotic diarrhea in
which a poorly absorbed solute is fermented into Short Chain
Fatty Acids which increase osmotic solute load as in Lactase
deficiency, such that diarrhea stops with fasting. An example of
this is Lactase deficiency. Diarrhea may also be due to increased
intestinal motility which decreases transit time as in the case of
Irritable Bowel Syndrome, or due to mucosal inflammation which
decreases the mucosal surface area for reabsorption as in cases
of Shigella, Rotavirus, Amebiasis.
Management is guided by the hydration status of the patient.
Patients may have no dehydration, some dehydration, or severe
dehydration based on clinical manifestations. Patients with some
dehydration are often restless and irritable, have sunken
eyeballs, dry buccal mucosa, absent tears, capillary refill time of
more than 2 seconds, and decreased urinary output but drink
eagerly in response to thirst. In comparison, patients with severe
dehydration have even worse symptoms and signs with the
distinguishing factors being lethargy, absent urine output, and
the poor urge to drink in response to thirst.
Patients with no dehydration may be managed at home using
Oral Rehydration Salts. The current standard ORS contains 75
meqs of glucose and sodium, 65 meqs of chloride, 20 meqs of
potassium, and 10 meqs of citrate, with a total osmolarity of 245.
ORS is given in a preparation of 1 sachet mixed with 200 ml of
water, and is given volume per volume loss. A homemade
preparation using 8 teaspoons of sugar with 1 teaspoon of salt
mixed in 200 ml water may be used as an alternative. ORS
treatment is continued for 2 days and should be supplemented
with breastfeeding, increased intake of bananas, fruits,
vegetables, meat, and fish. Patients should return to the
emergency room if resolution is not achieved within 3 days, or
immediately if symptoms worsen, fever develops, oral intake
cannot be tolerated, or there is blood in the stool. For patients
with some signs of dehydration, it is critical to deliver

an adequate amount of ORS over the 1st 4 hours of

management. Amount is calculated using the formula Weight x
0.75 ml and the amount is divided evenly over 4 hours. The
patient is closely observed over 4 hours and if oral intake is
tolerated and symptoms of dehydration improve home care
using the aforementioned plan is sufficient. For patients with
severe dehydration IV LRS or NSS should be started at a rate of
30 ml/kg over the first 30 minutes to 1 hour, then 70 ml/kg over 2.5
to 5 hours. Patient should be reassessed every 1 to 2 hours. If the
patient for whatever reason cannot immediately be given IV
fluids and oral intake is not tolerated a nasogastric tube can be
installed and ORS can be given at 20 ml/kg/hour for 6 hours.
These patients should be monitored for at least 6 hours.
Once steps for the management of dehydration have been
instituted laboratories and ancillaries may be requested in order
to pinpoint the cause of diarrhea as well as determine the extent
of losses due to dehydration. In patients with high fever, bloody
stools, and a more prolonged course of illness in whom a
bacterial cause is highly suspected fecalysis can be requested in
order to confirm this suspicion so that antibiotic therapy may be
initiated. Fecalysis can also reflect whether steatorrhea is present
reflecting the possibility of a malabsorption syndrome as the
cause of the diarrhea. In patients with severe dehydration in
whom electrolyte losses are suspected to be substantial, serum
sodium and potassium should be started so that the proper
intravenous fluid can be selected to achieve adequate
replacement.
Ideally, antimicrobial therapy should be targeted. In cases with
bloody stools in which Shigella is highly considered, Trimethoprim
+ Sulfamethoxazole is the agent of choice, alternatives include
Ampicillin and Nalidixic acid. In cases where in stools are
described as rice water like, Cholera should be suspected and
Tetracycline may be used. Infection with amoebiasis and
Giardiasis may be treated with Metronidazole. Fever should be
managed with antipyretics, and in those living in an area where
Falciparum malaria is endemic, malaria should be part of the
differentials.

13 HEPATIC ENCEPHALOPATHY
Hepatic encephalopathy is a state of disordered central nervous
system function resulting from the inability of the liver to
adequately detoxify noxious agents of gut origin secondary to
hepatocellular dysfunction and portosystemic shunting caused
by either an underlying chronic hepatic pathology or acute
hepatic failure. In the setting of acute hepatic failure, it is a
syndrome characterized by psychiatric as well as neurologic
abnormalities with jaundice manifesting within 2 to 8 weeks from
the onset of symptoms in the absence of any pre-existing liver
disease. The known etiologic factors of hepatic encephalopathy
include viruses such as Hepatitis, chemicals such as Ammonia,
drugs such as opioids and sedatives, and surgery, cancer, and
radiation. In the presence of chronic liver disease, precipitating
factors include azotemia, hypokalemia, high protein diet,
gastrointestinal bleeding, and hypovolemia.
Normally, ammonia is metabolized from dietary amino acids by
resident bacterial flora in the colon. The ammonia is reabsorbed
by the portosystemic circulation. 80 to 90% of the total ammonia
produced is shunted to the liver where it is detoxified into urea
and eventually excreted in urine. The remaining 10 to 20% is
shunted to the other ammonia metabolizing organs: the brain,
heart, and kidneys. When more than 60% of hepatic function is
lost or when portosystemic shunting towards the brain, heart,
and kidneys is present, there is failure of ammonia detoxification.
As ammonia levels rise, the brain, heart, and kidneys attempt to
compensate but eventually become overloaded and fail to
metabolize the overwhelming amount of ammonia, thus
hyperammonemia occurs. Ammonia exerts multiple neurotoxic
effects resulting to neurologic and psychiatric abnormalities.
The major clinical features of hepatic encephalopathy include:
altered
mental
status,
personality
changes,
neuroophthalmologic
changes,
motor
abnormalities,
and
electroencephalographic findings. Based on these clinical
features, hepatic encephalopathy may be classified to indicate
the severity of the disease. Grade I is separated from the more
severe stages by the presence of a normal EEG finding as well as
the motor abnormality being tremors only. Symptoms include a
sleep reversal pattern, emotional lability, irritability, and mild
confusion. Grade II and the succeeding stages are
characterized by abnormal EEG findings which reveal slow, high
amplitude, triphasic waves, as well as the presence of asterixis.
Grade II symptoms include lethargy, inappropriate behavior,
and disorientation. Grade III symptoms include somnolence,
aggressive behavior, and severe confusion. Lastly, Grade IV may
reveal a comatose patient with or without response to normal
stimuli. Because of the characteristic manifestations of hepatic
encephalopathy and the lack of any other specific diagnostic
modalities for the disease, diagnosis is often achieved clinically.
Since the main pathology in hepatic encephalopathy is the

elevation of ammonia levels treatment is geared towards

reducing ammonia formation. The mainstay of treatment in
hepatic encephalopathy continues to be intake of Lactulose, a
non-absorbable dissacharide that is metabolized into short chain
fatty acids by the resident bacterial flora in the colon which
results in acidification of the colonic environment favoring the
formation of Ammonium ion NH4 which compared to NH3 is nonabsorbable, non-neurotoxic, and is easily excreted in urine.
Lactulose also induces catharsis which promotes turnover of gut
flora, decreasing the number of ammonia forming flora. The
dose is 30 ml PO TID to QID and is titrated to achieve 3 to 5 soft
stools per day. Certain antibiotics can also be given in order to
promote turnover of gut flora. Traditionally, Neomycin an
aminoglycoside which interferes with bacterial protein synthesis
by binding to the 30S ribosomal subunit, is given alternatingly
with Metronidazole which inhibits nucleic acid synthesis by
disrupting DNA. These antibiotics are given alternatingly because
of their poor safety profile. Neomycin causes ototoxicity and
nephrotoxicity
while
Metronidazole
causes
peripheral
neuropathy. More recently, Rifaximin, a derivative of Rifampicin,
which binds to the beta subunit of bacterial RNA polymerase to
disrupt DNA formation, has been used for its better safety profile
at a dose of 550 mg BID PO. Dietary protein restriction is no
longer advised in hepatic encephalopathy as the ensuing
malnutrition has been found to outweigh any beneficial effects.
Restriction is reserved for the small subset of patients who
completely are unable to tolerate protein and often trial of
shifting to vegetable sources for protein is attempted before
complete restriction of protein in the diet. It is important to also
address
any
hypovolemia,
electrolyte
abnormalities,
gastrointestinal bleeding as these are the precipitating factors
for decompensation.

14 HYPERTENSIVE CRISIS
A hypertensive crisis is a sudden, acute blood pressure elevation
to levels higher than what is normal for the affected individual.
There are two types, the first is hypertensive urgency,
characterized by asymptomatic blood pressure elevation. The
second is hypertensive emergency, which in comparison is blood
pressure elevation with symptoms, signs, or laboratory findings
pointing towards end organ damage. Under hypertensive
emergency there are two further categories: Accelerated
hypertension which is characterized by headaches, blurred
vision, and focal neurologic deficits,
and Malignant
hypertension which is Accelerated hypertension with
papilledema. The most common end organ damage caused by
Hypertensive
emergencies
includes
hypertensive
encephalopathy, intracerebral hemorrhage, acute myocardial
infarction, left sided heart failure with concomitant pulmonary
edema, dissecting aortic aneurysm, and kidney injury or failure.
In 90% of cases, hypertensive crisis is a consequence of
uncontrolled longstanding primary or essential hypertension.
However, it may also be due to uncontrolled causes of
secondary hypertension such as renal parenchymal disease,
renovascular disease, pheochromocytoma, Cushings syndrome,
Primary Hyperaldosteronism, Coarctation of the aorta, and
obstructive sleep apnea.
Laboratories and ancillaries are requested with the goal of
determining the extent of end organ damage in order to guide
treatment decisions as certain organ dysfunctions can become
relative contraindications for starting certain antihypertensives. It
is imperative to request for a 12 lead electrocardiogram in order
to determine whether there is an ongoing myocardial infarction.
Biomarkers for myocardial infarction such as Troponin I should
also be requested if the patients clinical findings are suggestive.
ECG findings may also suggest the presence of electrolyte
abnormalities and cardiac chamber enlargement. Urinalysis
should be requested to screen for any hematuria or proteinuria
indicative of acute kidney injury, results should be correlated
with serum creatinine levels. Serum electrolytes should also be
measured not only to guide correction but also to guide the
choice of antihypertensive agent. A Chest X-ray should be
requested if pulmonary edema is a consideration in a patient
with equivocal chest physical examination findings.
Management goals are different for urgencies and
emergencies. In the setting of a hypertensive urgency, blood
pressure may be lowered over the course of the next 24 hours. In
comparison, blood pressure must be lowered by 25% over the
next 60 minutes in hypertensive emergency in order to lessen
end organ damage, and care must be taken to avoid
overzealous correction that can lead to sudden hypoperfusion
of the cerebral, coronary, and renal vascular beds. Oral
antihypertensives may be sufficient in cases of urgency.

Clonidine, Captopril, and Nifedipine are the most common

agents used. Parenteral antihypertensives are indicated in
Emergencies and current guidelines suggest the use of
Nicardipine as the first line agent. It is the most potent and
longest acting of the parenteral calcium channel blockers.
Diuretics such as Furosemide may be added for patients with
features of heart failure or fluid retention. Target blood pressure is
160/100 mmHg until resolution of symptoms.

17 VENOUS THROMBOEMBOLISM
Venous thromboembolism is a disorder characterized by acute
pulmonary embolism and deep vein thrombosis. Pulmonary
embolism on the other hand, is not a disease per se but a
complication of a disease, commonly venous thrombosis
occurring in the deep veins of the lower extremities. Thrombus
formation and subsequent pulmonary embolism are associated
with three basic factors: stasis, hypercoaguability, and
endothelial injury which make up Virchows triad.
Venous thrombi form either in the vicinity of a venous valve
where eddy currents arise or at the site of intimal injury. Platelets
aggregate with the release of mediators of the coagulation
cascade, forming a red thrombus. At any time, a part of or even
the entire thrombus may detach as an embolus which can
lodge anywhere in the pulmonary vasculature or even the heart.
In the lungs it leads to impaired gas exchange, increased
pulmonary vascular resistance. Often acute pulmonary
embolism results from emboli originating from the proximal veins
of the lower extremities, above the popliteal vein. In comparison,
majority of thrombi arising below the level of the popliteal vein
resolve spontaneously and do not commonly embolize.
The most frequent symptom is dyspnea while the most frequent
sign is tachypnea. Classic signs of pulmonary embolism include
low grade fever, neck vein distention, and an accentuated
pulmonic component of the second heart sound. Hypotension
and cyanosis may indicate massive pulmonary embolism while
pleuritic pain, cough, or hemoptysis may suggest a smaller
embolism. Majority of patients may not present with any leg
symptoms and often the clinical manifestations are insufficient to
confidently rule in or rule out venous thromboembolism. Wells
Criteria may be used to guide management. It is comprised of
the following variables: presence of active cancer, signs and
symptoms of DVT, PE is more likely than an alternative diagnosis,
tachycardia, surgery or immobilization in the previous 4 weeks,
prior DVT or PE, and hemoptysis. A score of 3 or more suggests
high probability of venous thromboembolism.
In terms of laboratories and ancillaries for diagnosis, pulmonary
angiography remains the gold standard for the diagnosis of
pulmonary embolism which in consistent with finding of a filling
defect or sharp cutoff of small vessels. Contrast venography on
the other hand is the gold standard for diagnosing deep venous
thrombosis. When these are not immediately available or
feasible a Duplex scan can be used to investigate for deep
venous thrombosis and a Chest X-ray may yield findings of
pulmonary embolism such as Hamptons hump which is a
wedge shaped infiltrate, Westermarks sign which is decreased
pulmonary vascularity, and Pallas sign which reflects an
enlarged right descending pulmonary artery. A D-dimer assay in
combination with the Wells Clinical Prediction Rule is effective in
ruling out clinically significant pulmonary emergency.

Treatment is geared towards resolving the ongoing embolism

and prevention of further embolism episodes. Thrombolytic
therapy may be instituted using Streptokinase, Urokinase, and
recombinant Tissue Plasminogen Activator. Further clot formation
in the lower extremities may be prevented by anticoagulant
therapy with unfractionated heparin which is the initial drug of
choice, warfarin, low molecular weight heparin (Enoxaparin).

20 HEMOPTYSIS
Hemoptysis is the expectoration of blood from a source below
the glottis often following coughing spells. It can be caused by
several factors: infections such as pulmonary tuberculosis,
paragonimiasis, bronchiectasis, neoplasms such as bronchial
carcinoma, cardiovascular conditions such as mitral stenosis,
acute
pulmonary
edema,
aortic
aneurysm
rupture,
thromboembolism, trauma, and iatrogenic factors such as
endotracheal
intubation,
pulmonary
catheterization,
bronchoscopy, percutaneous lung biopsy. In 20% of cases the
cause may remain unknown despite extensive evaluation, and
are termed Cryptogenic hemoptysis.
Clinical manifestations depend on the primary disease, site,
degree, and rate of hemorrhage. Minor hemoptysis may present
with just blood streaked sputum, with or without discomfort or
bubbling sensation over the chest. Massive hemoptysis, defined
as expectoration of 200 to 600 ml of blood over 24 hours may
present with signs and symptoms of asphyxiation and
hemodynamic alterations.
Work-up includes a complete otorhinolaryngeal examination
with rhinoscopy and nasopharyngeal and laryngeal endoscopy,
to rule out any upper airway sources of bleeding. A chest X-ray
may be requested to determine whether a pulmonary
pathology is the most likely cause. AFB and gram staining of
sputum are also indicated to search for the root cause of
hemoptysis. In patients with persistent mild bleeding in whom
bed rest and antitussives such as Dextromethorphan and
Benzonatate, are insufficient to provide relief, fiber
bronchoscopy may be performed to localize the source of
bleeding. A rigid scope may be used for massive bleeding to
provide for better visibility, suctioning, and airway control. Once
the source of bleeding has been located suctioning or lavage,
endobronchial tamponade may be attempted. Resectional
surgery may be performed in severe cases while arterial
embolization may be performed if surgery is contraindicated. If
the source still cannot be identified bronchial arteriography or
pulmonary arteriography may be indicated. The airway must be
maintained patent at all times as asphyxiation poses a greater
threat than blood loss.

21PNEUMOTHORAX
Pneumothorax is a collection of air or gas in the pleural space
that increases intrapleural pressure causing overexpansion of the
hemithorax and varying degrees of lung collapse. It is termed
Spontaneous pneumothorax if it occurs in the without
antecedent trauma or iatrogenic cause and may be primary or
secondary. Primary spontaneous pneumothorax occurs without
a clinically apparent underlying lung disease in a patient with risk
factors such as family history of pulmonary pathology and
smoking. This is common in tall, thin men in their 20s and is
thought to be due to the rupture of pleural blebs or bullae. In
comparison, the secondary type is due to an underlying
pulmonary pathology, the most common of which is airway
obstruction secondary to chronic obstructive pulmonary disease,
other examples include infections such as pulmonary
tuberculosis, and necrotizing pneumonia, neoplasms that may
be primary or metastatic, interstitial lung disease, trauma, or
iatrogenic as in during cardiopulmonary resuscitation,
mechanical ventilation, endotracheal intubation, and other
diagnostic or therapeutic interventions. Tension pneumothorax
occurs when the pressure build up forces the lungs to collapse
such that venous return is impeded and the heart is prevented
from pumping blood effectively.
Clinical manifestations are apparent even in minimal (less than
or equal to 3 cm) pneumothorax. Symptoms include sudden
sharp chest pain worsened by deep breathing or cough, often
localizing to the affected side, dyspnea or chest tightness, easy
fatigability, and in cases of impending cardiopulmonary failure:
cyanosis, and hemodynamic and cognitive abnormalities. On
physical examination the hemithorax of the affected side may
be noted to be over-expanded, lagging, tympanitic, with
decreased to absent breath sounds and fremiti. The midline
mediastinal structures and trachea may also shift to the opposite
side. In tension pneumothorax the neck veins may be distended
and hypotension may be noted. Subcutaneous crepitations and
emphysema, facial and neck edema are other signs.
Diagnosis may be confirmed via Chest X-ray which will reveal a
Visceral Pleural Line as well as atelectasis and mediastinal or
tracheal shift to the opposite side. Subcutaneous emphysema or
pneumomediastinum may also be visualized if present.
Additional ancillaries include Chest CT scans for cases of
secondary spontaneous pneumothorax whose underlying
etiology is unknown.
Needle aspiration can be performed in the emergency room to
resolve this emergency. The patient is placed in a semirecumbent position. The area of the 2nd LICS MCL is sterilized and
infiltrated with 1 to 2% lidocaine up to the parietal pleura. A 14 to
16 gague cannula is inserted through the parietal pleura and
connected to a stopcock at which point air is aspirated gently.
The procedure is stopped once resistance is felt.

22 SUBMERSION INJURY
Near drowning is defined as survival of 24 hours or more after
suffocation by submersion in a liquid medium of sufficient severity
that leads to morbidity or death. In comparison, drowning is the
mortal submersion event in which the victim dies within 24 hours.
Near drowning has been replaced by the term Submersion injury
to connote the event until the time of drowning related death.
Submersion injury may be classified depending on the
temperature of the liquid medium into warm-water drowning
occurring in temperatures of 20C or higher, cold-water drowning
occurring in temperatures of less than 20C, and very cold-water
drowning as in temperatures of 5C or less. The temperature of
the liquid medium is important because hypothermia adds
significant risk for developing further complications.
Immersion in a liquid medium stimulates hyperventilation, the
resulting gasping and possible aspiration then trigger voluntary
apnea and laryngospasm which results in hypoxemia and a
concomitant acidosis. The hypoxemic and acidotic environment
depletes the cerebral and coronary vascular beds of oxygen
supply such that cerebral ischemia and cardiac arrest develop.
Eventually asphyxia sets in which in most cases leads to a
relaxation of the airways permitting the lungs to take in water. In
10 to 20% of cases laryngospasm is maintained such that there is
dry drowning. Clinical manifestations depend on the severity
of pulmonary, cardiovascular, and/or neurologic damage.
Some patients may be asymptomatic while others may present
with hypothermia, tachycardia, bradycardia, tachypnea,
dyspnea, wheezing, crackles, altered mental status, and
neurologic deficits. Some may present with features of
cardiopulmonary arrest: apnea, asystole.
Management is divided into 3 phases: pre-hospital care, ER unit
care, and in-patient care. At the scene of the drowning the
patient must immediately be removed from the water with
adequate support given to the neck in case of cervical spinal
cord injury. The patient is then assessed for the need for
cardiopulmonary resuscitation. Chest compressions are then
initiated immediately if indicated. 100% supplemental oxygen by
face mask should also be given, early intubation may be
considered in patients that continue to be hypoxemic. The
patient should also be rewarmed thus all wet clothing must be
removed and warm blankets should be used for drying and
insulation. In the ER unit, endotracheal intubation is performed
on those unable to maintain an arterial oxygen partial pressure
of more than 60 to 70 mmHg, or in those with an altered level of
consciousness leading to inability to protect airway or handle
secretions, and those with worsening ABG results. At this point
other than ABG, tests should be ordered to rule out any other
injuries. Cranial CT scan, cervical spine radiograph, Chest X-ray,
and scout film of the abdomen may be ordered if indicated.
ECG and serum electrolytes may also provide information on the

severity of the submersion injury and guide the manner of

replacement fluid therapy. Thermoregulation should be ensured.
In patients who fail to warm up despite use of heating pads,
warm air, or warm baths, pleural and peritoneal irrigation,
continuous arteriovenous rewarming, hemodialysis, and
cardiopulmonary bypass may be warranted. In the in-patient
setting bronchospasm should be relieved with a bronchodilator,
antibiotics should be instituted in those who were submerged in
contaminated water, or in those with fever, new pulmonary
infiltrates, or purulent secretions.
Early complications include bronchospasm, hypothermia,
seizures, hypovolemia, fluid and electrolyte disturbances, and
metabolic and lactic acidosis. Late complications include
respiratory distress syndrome, ischemic encephalopathy,
aspiration pneumonia, lung abscess, pneumothorax, renal
failure, sepsis, and barotrauma.

24 ADRENAL CRISIS
Adrenal crisis is an extreme decompensated form of adrenal
insufficiency characterized by a deficiency in glucocorticoids
with or without a deficiency in mineralocorticoids leading to a
decrease in vascular sensitivity to norepinephrine and
angiotensin II such that peripheral adrenergic tone is reduced
leading to vascular collapse and shock. Any disorder affecting
the
hypothalamic-pituitary-adrenal
axis
resulting
to
glucocorticoid deficiency can give rise to adrenal insufficiency.
And depending on which level is affected the disorder can be
categorized into primary, secondary, or tertiary adrenal
insufficiency. Primary adrenal insufficiency or Addisons disease is
a dysfunction or complete absence of the adrenal cortex such
that not only is there a deficiency in glucocorticoids but also a
concomitant deficiency in mineralocorticoids. Because of this,
an additional dysfunction in the renin-angiotensin-aldosterone
system is present thus crisis secondary to Addisons disease is
often more common and more severe. In developed countries,
autoimmune pathologies most commonly cause Addisons
disease, in comparison, in developing countries such as ours,
infections commonly are the cause. In particular tuberculosis is
the most common etiology of primary adrenal insufficiency in our
country. Secondary adrenal insufficiency is any pathology
affecting the pituitary gland such as a mass lesion. Tertiary
adrenal insufficiency is any pathology affecting the
hypothalamus. Other predisposing factors include the sudden
withdrawal of steroid therapy, and any stress inducing event
such as a major systemic illness, surgery, and adrenal
hemorrhage.
A patient with adrenal crisis may present in the ER with
hypotension, tachycardia, and shock disproportionate to the
severity of the current illness. They may also present with a history
of nausea and vomiting with a background of weight loss and
anorexia. The patient may also complain of abdominal pain,
fever especially in those caused by infections, and
hyperpigmentation in those with primary adrenal insufficiency. A
patient presenting with purpura known to have adrenal
insufficiency should raise suspicion adrenal infarction in
Waterhouse
Friedrichsen
Syndrome
secondary
to
meningococcemia. Laboratories may reveal unexplained
hypoglycemia, hyponatremia, hyperkalemia, hypercalcemia,
azotemia, and eosinophilia. Because the clinical manifestations
of adrenal crisis are nonspecific it is important to request for the
proper laboratories and ancillaries to clinch the diagnosis.
Since the pathology is basically glucocorticoid deficiency,
cortisol levels should be investigated in order to determine the
presence of this condition. Normally cortisol levels peak during
early morning and during periods of stress. As such levels less
than 5 ug/dl are suggestive of insufficiency but levels of up to 10
ug/dl still make an individual highly suspect. Levels of 20 ug/dl or

higher
preclude
the
diagnosis.
A
250
ug
short
adrenocorticotrophic hormone stimulation test can also be
performed. An increase of 10 ug/dl from baseline and an
absolute cortisol level greater than 20 ug/dL an hour after
administration rules out primary adrenal insufficiency but cannot
completely eliminate the possibility of secondary adrenal
insufficiency especially of recent onset.
It must be emphasized however that management should not
be delayed while waiting for the results of the laboratories
requested for. Intravenous access must be gained immediately,
and IVF should be started with PNSS. Intravenous Hydrocortisone
or Dexamethasone should then be started immediately.
Vasopressors and oxygen as well as other supportive measures
should be instituted as indicated. Once the patient is stable
further laboratories can be requested to determine the exact
etiology of the adrenal insufficiency. Fludrocortisone may be
given in those with concurrent mineralocorticoid deficiency.
Glucocorticoids should be tapered to maintenance dosage
over 1 to 3 days once appropriate.

25 DIABETIC KETOACIDOSIS
Diabetic ketoacidosis is an extreme decompensated state of
diabetes mellitus characterized by the triad of hyperglycemia of
more than 250 mg/dl, ketosis as reflected by positive urine
ketones, and high anion gap metabolic acidosis as reflected by
a pH of less than 7.3 and an anion gap of more than 10. It is
often precipitated by sudden discontinuation of insulin,
infections, cerebrovascular accident, myocardial infarction,
sympathomimetics, and pancreatitis.
Diabetic ketoacidosis is a state of decreased net effective
action of circulating insulin such that glucose utilization is
decreased creating a state of relative starvation, stimulating the
release of counter-regulatory hormones such as Glucagon,
Cortisol, Catecholamines, and Growth Hormone which promote
processes that increase blood glucose levels to maintain cellular
function such as Gluconeogenesis and Glycogenolysis. Lipolysis is
also stimulated such that adipose is converted into free fatty
acids which accumulate and are oxidized into ketones because
they are unable to enter the citric acid cycle without insulin. The
kidneys attempt to filter the excess highly osmotic glucose
leading to severe dehydration and in compendium with ketosis,
serum electrolyte derangement.
Patients
usually
present
with
polyuria,
polydipsia,
nausea/vomiting, abdominal pain, dehydration, hypotension,
mental status changes, Kussmauls breathing, and acetone
breath.
Diagnostic tests are aimed towards evaluating the severity of the
disease. Plasma glucose, arterial blood gas, urine ketones, serum
sodium, potassium, and chloride, and blood urea nitrogen as
well as creatinine are important in classifying the severity. Mild
DKA is characterized by a pH of less than 7.3, serum bicarbonate
of less than 18, anion gap of more than 10, and clinically an alert
individual. In comparison, severe DKA is characterized by an
arterial pH of less than 7, serum bicarbonate of less than 10,
anion gap of more than 12, and an individual who has
depressed mental status of stupor or coma. Anything in between
is moderate DKA. The precipitating cause should also be
investigated so that it can be treated to prevent further
exacerbation. ECG should be requested, as well as CBC,
Urinalysis, and Chest X-ray.
Hypovolemia and vascular collapse are the most common
cause of death in uncomplicated ketoacidosis as such
correction is an urgent therapeutic priority. In the absence of
heart failure, isotonic saline can be infused at 15 20 ml/kg/h or
greater during the 1st hour. Before instituting insulin treatment,
hypokalemia must be ruled out because insulin can exacerbate
this. Potassium levels must be normalized before starting insulin.
Once the patient is normokalemic, the treatment of choice
except in mild DKA is continuous IV infusion of Insulin aimed
towards decreasing glucose at a rate of 50 to 75 mg/dl/hour.

An initial bolus of 0.15 U/kg followed by infusion rate of 0.1

U/kg/hour can be used. When glucose reaches 250 mg/dl, rate
can be decreased to 0.05 to 0.1 U/kg and Dextrose may be
added until acidosis resolves. Treatment goal is glucose of less
than 200 mg/dl, serum bicarbonate of more than 18 meq/L, pH
of more than 7.3, and anion gap of less than 12 meq/L. Once this
is achieved, insulin infusion maybe discontinued and shifted
towards maintenance dosing.

26 THYROID STORM
First we define three important terminologies. Hyperthyroidism
refers to excess circulating thyroid hormone resulting only from
thyroid gland hyperfunction. Thyrotoxicosis refers to excess
circulating thyroid hormone resulting from any cause including
thyroid hormone overdose. Thyroid storm refers to the extreme
manifestation of thyrotoxicosis, an acute severe, life-threatening
hypermetabolic state causing adrenergic hyperactivity or
altered peripheral response to thyroid hormone. It most usually
occurs when an already thyrotoxic patient suffers a serious
concurrent illness, event, or injury such a infection, stress,
myocardial infarction, or trauma that frees thyroid hormones
from their binding sites or increases receptor sensitivity such that
the effect of thyroid hormones is multiplied. Manifestations
include high fever, cardiac findings such as tachycardia out of
proportion to fever, mental status changes, gastrointestinal
symptoms such as diarrhea, abdominal pain, generalized
weakness, palmar erythema.
Management goals include supportive care by giving
Acetaminophen for fever, normal saline or LRS for volume
depletion, inhibition of new thyroid hormone synthesis by giving a
Thionamide such as Methimazole or propylthiouracil, inhibition of
thyroid hormone release by giving iodine in the form of
potassium iodide or Lugols solution, blocking beta adrenergic
receptors by giving propranolol, and preventing peripheral
thyroxine conversion to triiodothyronine by giving intravenous
hydrocortisone or dexamethasone. It is also important to address
the precipitating event.

29 ANIMAL BITES
Rabies is a 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 such as
cats and dogs. There are two types, Vesiculovirus which is selflimited and mild, and Lyssavirus which leads to serious neurologic
disease. The virus remains in the site of entry during the
incubation period which may last anywhere from 20 to 90 days.
Eventually, the virus binds to nicotinic ACh receptors on
postsynaptic membranes at neuromuscular junctions where they
replicate and spread centripetally via retrograde axonal
transport along the peripheral nerves to the spinal cord or
brainstem where further dissemination takes place especially in
neurons. Centrifugal spread then occurs along sensory and
autonomic nerves towards the tissues of the salivary glands,
heart, adrenals, and skin.
Clinical manifestations progress from a flu-like prodrome of fever,
malaise, anorexia, and pain and pruritus in the wound site, to the
encephalitic phase characterized by anxiety, agitation,
hydrophobia, bizarre behavior, and other autonomic
dysfunction, to the paralytic phase characterized by flaccid
paralysis of the limbs to quadriparesis with facial paralysis, until
eventually coma or death ensue. As of current no diagnostic
tool is of use in confirming rabies, as such treatment must be
instituted once clinical suspicion for the disease arises.
First, proper wound cleaning must be performed. The wound
must be vigorously washed and flushed with soap or detergent
and water for at least 10 minutes. Alcohol, povidone iodine, or
any other antiseptic may also be used. For frankly infected
wounds, open wounds, bleeding wounds, antimicrobials in the
form of co-amoxiclav or cefuroxime may be started. Anti-tetanus
immunization should also be given. The category of the wound
should also be established. Category I includes having intact skin
licked by an infected animal, sharing eating or drinking utensils
with an infected patient. This category requires only local wound
treatment. Category II includes uncovered skin nibbled or
nipped by an infected animal resulting to bruising, minor
scratches or abrasions without bleeding, licks on broken skin, and
wounds induced to bleed. This category indicates immediate
start of active vaccination. If the animal remains alive and well
for 14 days, vaccination may be discontinued after the Day 7
dose. However if the animal becomes rabid, dies, or
in
unavailable for 14 days or tests positive for rabies, the complete
regimen until Day 30 should be given. Lastly, Category III includes
transdermal bites or scratches, contamination of mucuous
membranes with saliva, exposure to rabies patients through
bites, mucous membrane, or open skin lesions, handling infected
carcass or ingestion of raw infected meat, and all Category II
occurring in the head and neck. This category merits both active
immunization and passive immunization products.

30 TETANUS
Tetanus is an acute, often fatal disease caused by wound
contamination with Clostridium tetani, a motile nonencapsulated anaerobic gram positive rod. Clostridium tetani
exists in either a vegetative or spore forming state. The spores are
ubiquitous in soil and animal feces and are extremely resistant to
destruction, surviving on environmental surfaces for many years.
Usually, it is introduced into a wound in the spore-forming noninvasive state, however it can germinate into the toxin
producing vegetative form if tissue oxygen tension is reduced as
in presence of crushed, devitalized tissue, presence of a foreign
body, or development of another source of infection. It
produces two exotoxins, the first is tetanolysin which favors
expansion of the bacterial population, and the second is
tetanospasmin, a powerful neurotoxin that reaches the central
nervous system via hematogenous spread to the peripheral
nerves and retrograde transport. It acts on the motor end plates
of the skeletal muscles, in the spinal cord, brain, and
sympathetic nervous system. It prevents the release of inhibitory
neurotransmitters glycine and gaba aminobutyric acid from
presynaptic nerve terminals thus releasing the nervous system
from its normal inhibitory control. This leads to the clinical
manifestations of tetanus such as generalized muscular rigidity,
violent muscular contractions, and autonomic instability. There
are three forms of the disease. The first is generalized tetanus
which is the most common. Patients present with pain and
stiffness of the masseters or lock jaw, later becoming rigidity
hence development of trismus and risus sardonicus. Dysphagia,
opisthotonus, clenching of the fists, extension of lower extremities
result as a consequence of reflex convulsive spasms and tonic
muscle contractions. Mental status is normal. In comparison
cephalic tetanus results to dysfunction in the cranial nerves most
commonly the 7th. Lastly local tetanus is manifested by rigidity of
muscles in proximity to the site of inoculation.
Diagnosis is achieved clinically. Treatment is instituted with
Tetanus immunoglobulin to neutralize circulating tetanospasmin,
administered opposite the site of tetanus toxoid administration.
Wound management is then performed and muscle relaxants
are given such as benzodiazepines such as Midazolam.
Neuromuscular blockade can also be attempted by using
succinylcholine or vecuronium. Autonomic dysfunction may be
treated with magnesium sulfate which inhibits epinephrine and
norepinephrine release, Labetalol which has alpha and beta
adrenergic blocking activity, and clonidine which is an alpha 2
receptor agonist. Tetanus toxoid should be given after recovery
because the disease does not confer immunity.