EMERGENCIES Scripts for Memorization Mikatron Scissored

7/25/2019 EMERGENCIES Scripts for Memorization Mikatron Scissored

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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 ofthe 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 Guidelinesrecommends 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 otherhand on the sternal notch, position the shoulders over

hands with elbows locked and arms straight

!Push hard and push fast: 100 compressions/minutewith a

depth of at least 2 inchesor 5 cm

!Allow complete recoilof 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 orjaw 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 secondsand 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


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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 andaryepiglottic 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

CHRONIC CAUSES

LARYNGO-

TRACHEO-

BRONCHITIS

EPIG

LOTTITIS

BACTERIAL

TRACHEITIS

RETRO-

PHARYNGEAL

ABSCESS

PERITO

NSILLAR

AB

SCESS

Airwayswellingin

thesupraglottic

andglotticarea

usuallysecondary

toaviralcause

Infec

tionof

theepiglottis

and

arye

piglottic

foldsand

surro

unding

softtissue

Acute

bacterial

infectionof

theupper

respiratory

tract

Infectionofthe

potentialspace

betweenthe

posterior

pharyngealwall

andprevertebral

fascia

Infectionofthe

poten

tial

space

betwe

enthe

superior

constrictorand

tonsils

Parainfluenza1,3

RSV,Influenza,

Adenovirus

Hib

GBSt

rep

S.pneumoniae

S.aureus

S.aureus

Hib

GAStrep

Anaerobes

S.aureus

GAStre

p

Anaero

bes

Coryza

Fulm

inant

Resp

iratory

distress

Sniffing

position

Highfever

Respiratory

distress

Neckstiffness

Bulgingneck

mass

Gurgling

respiration

Severethroat

pain

Trismus

Tortico

llis

Hotpotato

voice

X-ray:Subglottic

narrowing

(SteepleSign)

CBC

,X-ray:

Swollen

epig

lottis

(ThumbSign)

CBC,Xray:

Ragged

irregular

tracheal

border

CBC,X-ray:

Thickened

retropharyngeal

space

CBC

Endos

copy

Mistvaporizer

Racemic

Epinephrine

Dexamethasone

Intub

ation

Cefo

taxime,

Ceft

riaxone,

Amp

i-Sul

Cefotaxime,

Ceftriaxone,

Ampicillin-

Sulbactam

Antibiotics

Surgical

drainage

Antibiotics

Surgic

al

draina

ge

FOREIGN BODY

ASPIRATIONANGIOEDEMA SPASMODIC CROUP

Large foreign body

lodges in the larynx,

trachea, or bronchus

causing obstruction

Acute laryngeal

swelling causing

obstruction

Airway swelling in the

supraglottic and glottic

area secondary to a

non-infectious cause

(allergic, psychologic)

Choking, gagging

Wheeze

Anaphylactic

shock:Pruritus

Urticaria

Swelling of the

lips, tongue

Coryza

X-ray

Bronchoscopy:

Diagnostic and

therapeutic

X-ray: subglottic

narrowing

X-ray: Subglottic

narrowing

Infants: 5 interscapular

back blows with childs

head lower than chestalternating with five

chest compressions

Older: Heimlich

maneuver

Epinephrine

IVF

Steroids

Cool mist

CHOANAL

ATRESIA

LARYNGOMALACIA/

TRACHEOMALACIA

VASCULAR

ANOMALIES

Persistence of

the buconasal

membraine inthe posterior

margin of hard

palate

Most common

congenital

anomaly of

nose

Laryngomalacia defect or

delayed maturation of

supporting structures of larynxcausing prolapse of epiglottis,

arytenoids, aryepiglottic folds

Tracheomalacia inadequate

cartilaginous and myoelastic

elements supporting trachea

leading to abnormal tracheal

collapse

Variation in

normal vascular

anatomycausing

obstruction of

the trachea or

bronchus

Unilateral:

Mucoid

rhinorrhea,

sinusitis

Bilateral:

Apnea,

cyanosis, RD

Worsens with crying, exertion,

feeding

Improves with prone position or

neck extension

Worsens with

feeding

Improves with

neck extension

Inability to pass

nasal catheter

High resolution

CT scan

Endoscopy: Flabby supraglottic

structures/anterior collapse of

trachea

Endoscopy

CT scan

Surgery Reassurance and respiratory

support

Resolves spontaneously by 24

months, if not:

Tracheobronchomalacia

requiring surgery

Surgery


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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 paralysis6. 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 hyper-

responsiveness to provocative exposures or triggers.

Acute asthma exacerbationis 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-IgE-

mediated 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, andexcess 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 pulmonaryvasoconstriction, 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, pulsusparadoxus, 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 airwayobstruction is responsive to a bronchodilator, which is suggestive

of asthma.


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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 agonistsuch 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 bymanifesting 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


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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 ofhypothermia. 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 cyanosisis 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 initiatedwith 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, ordiaphragmatic hernia. In the setting of pneumothorax, needle

aspiration using a 20 gauge needle inserted at the 4thICS AAL or

2ndICS 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.


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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 reactionis 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 1st5 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 Lactasedeficiency, 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 sunkeneyeballs, 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 intakecannot be tolerated, or there is blood in the stool. For patients

with some signs of dehydration, it is critical to deliver


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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 inorder 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 Shigellais 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 ammoniaproduced 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 neurotoxiceffects resulting to neurologic and psychiatric abnormalities.

The major clinical features of hepatic encephalopathy include:

altered mental status, personality changes, neuro-

ophthalmologic 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 diagnosticmodalities for the disease, diagnosis is often achieved clinically.

Since the main pathology in hepatic encephalopathy is the


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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 NH4which compared to NH3is non-

absorbable, 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 peripheralneuropathy. 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 alsoaddress 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 orderto 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 hypoperfusionof the cerebral, coronary, and renal vascular beds. Oral

antihypertensives may be sufficient in cases of urgency.

Clonidine Captopril and Nifedipine are the most common 17 VENOUS THROMBOEMBOLISM


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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 valvewhere 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 toconfidently 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 fillingdefect 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 incombination with the Wells Clinical Prediction Rule is effective in

ruling out clinically significant pulmonary emergency.

Treatment is geared towards resolving the ongoing embolism 20 HEMOPTYSIS


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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 thecause 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 ofbleeding. 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 22 SUBMERSION INJURY


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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 otherdiagnostic 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. Onphysical 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 semi-

recumbent position. The area of the 2ndLICS 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 andconnected 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 oxygensupply 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 ofcardiopulmonary 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 24 ADRENAL CRISIS


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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 Addisonsdisease, 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 lessthan 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 25 DIABETIC KETOACIDOSIS


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g p g g

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.

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 aswell 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 aimedtowards 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 26 THYROID STORM


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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.

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 seriousconcurrent 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 30 TETANUS


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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 self-

limited 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 infectedwounds, 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 immediatestart 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.

Tetanus is an acute, often fatal disease caused by wound

contamination with Clostridium tetani, a motile non-

encapsulated 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 non-

invasive 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 inhibitoryneurotransmitters 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 extremitiesresult 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.

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