Emergencies Reviewer

8/19/2019 Emergencies Reviewer

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4 PERINATAL ASPHYXIA s

Definition[1]

Interference in gas exchange between the organ systems of the

mother and fetus resulting in impairment of tissue perfusion and

oxygenation to vital organs of the fetus such that arterial carbon

dioxide partial pressure rises, and arterial oxygen partial pressure

and pH fall. When the arterial oxygen partial pressure is very low,

anaerobic metabolism occurs producing large quantities of

metabolic acids.

Epidemiology

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

period in 2008; in the same period asphyxia was the cause of

9% of all under five deaths [4]

•

Incidence[5]

! Resource-rich countries: 1/1000 live births

! Resource-poor countries: 5 – 10/1000 live births

Etiopathogenesis [1]

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

endothelial cells) imbibe fluid and swell, with a corresponding

reduction in ECF space

Vasogenic edema – increased capillary permeability leads to

escape of plasma infiltrate into the intracellular space through

incompetent tight junctions

Etiology – 5 causes during labor and delivery:

1. Interruption of umbilical blood flow (e.g. cord compression)

2.

Failure of gas exchange across the placenta (e.g. placenta

abruption)3.

Inadequate perfusion of the maternal side of the placenta

(e.g. severe maternal hypotension)

4.

A compromised fetus who cannot further tolerate the transien

intermittent hypoxia of normal labor (e.g. anemic, growth-

retarded)

5. Failure to inflate the lungs and complete the change in

ventilation and lung perfusion that must occur at birth

Clinical manifestations – Criteria for diagnosis:

1.

Fetal acidosis (pH < 7.0 or Base excess > 12 mmo/L)

2. APGAR score of 0 – 3 at 5 minutes

3.

Seizure

4. Multi-system organ dysfunction

APGAR SCORE[3]

•

Objective measurement of the newborn’s condition andresponse to resuscitation normally assigned at 1 minute and

again at 5 minutes

•

NOT used alone to determine the NEED for resuscitation or to

guide the resuscitation efforts

•

Resuscitation must NOT be delayed for the purpose o

tabulating APGAR score

PARAMETER SCORE 0 SCORE 1 SCORE 2

Color Blue, paleBody pink, extremities

blueTotally pink

Muscle toneNone,

limpSlight flexion

Active, good

flexion

Heart rate 0 < 100 > 100

Respiration Absent Slow, irregular Strong, regular

Reflex

irritabilityNone Some grimace

Good grimace,

crying

•

Interpretation of 1 minute APGAR score:

! > 7: requires minimal resuscitation other than drying and

stimulation! 4 to 6: mild to moderate asphyxia, more vigorous

resuscitation may be required (supplemental oxygen

vigorous stimulation)

! < 3: moderate to severe asphyxia, aggressiveresuscitation should be started immediately

INTRAPARTUM ASPHYXIA

Hypoxia

Aerobic

metabolism Hypercapnea

Anaerobic

metabolism

IncreasedLactate

Decreased pH

Redistribution of blood flow

Decreased:

Lungs

Kidneys

GI tract

Increased:

Heart

Brain

Adrenals

Ox en debt to the brain

Altered brain H20

distribution

Altered brain

cerebral blood flow

Cytotoxic

edema

Vasogenic

edema

Multifocal tissue

ischemia

Brain swelling Generalization


2/24

Management

American Academy of Pediatrics and American Heart Association

Algorithm for Neonatal Resuscitation[3,7]

Birth

No

Apneic or HR < 100 Breathing, HR > 100but cyanotic

Persistently cyanotic

HR < 60 HR < 60

HR < 60 HR < 60

1.

Temperature Control

• Newborns are at risk for hypothermia following delivery

because of their,

! Large surface area to mass ratio! Evaporative heat loss

• Hypothermia can lead to:

! Hypoglycemia

! Increased oxygen consumption

! Respiratory depression and acidosi

(if severe)

• Dry infant with warm towels and place infant unde

radiant heat source• Very low birth weight infants (< 1,500 g) are especially

prone to hypothermia and may need to be placed unde

plastic wrapping to avoid evaporative loss

•

Avoid hyperthermia as this may worsen ischemic brain

injury

2.

Positioning

• Place head into a “sniffing” position

! This position aligns the posterior pharynx, larynx, andtrachea, and allows for unimpeded air entry

! NOTE: Excessive extension or flexion of the neck may

result in airway occlusion

• Perform oral and nasal suctioning with a bulb syringe o

suction catheter

3. Stimulation

•

For vigorous newborns, drying and suctioning of the

mouth are usually adequate to increase heart rate andrespiratory effort

• If respiration is not adequate, flick the soles of the feet o

rub the infant’s trunk

• If no response is observed to tactile stimulation, initiate

Positive Pressure Breaths

4. Meconium

• VIGOROUS newborns do NOT require endotrachea

suctioning of meconium

• Indication for endotracheal suctioning of meconium

DEPRESSED newborns

! Absent or depressed respirations

! Heart rate < 100 bpm

! Poor muscle tone

•

Reassess newborn’s clinical status after every attempt

! Institute PPV if infant becomes severely depressed obradycardic

5.

Oxygen

• ALL infant with central cyanosis (mouth and tongue

should be provided free-flow oxygen even if they presen

only with mild respiratory distress

•

Acrocyanosis (hands and feet) represents periphera

vasoconstriction and is NOT an indication for oxygen•

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

bag mask held over the infant’s nose

6.

Ventilation

• Indications:

! Infant remains apneic or gasping

! Heart rate < 100 bpm after 30 seconds of initia

resuscitation

! Central cyanosis DESPITE supplemental oxygen•

Technique! Possible routes:

(1) Cushioned mask with a flow inflating bag

(2)

T-piece connector

! Use 100% oxygen, or room temperature PPV (i

unavailable)

! Peak pressure set up to 40 cm H2O due to “stiff” fluidfilled lungs of newborns, lower once fluid begins to

express from the lungs to avoid iatrogenic

pneumothorax

•

Bag-mask ventilation at 40 – 60 breaths per minute is

continued for 30 seconds, then infant is reassessed

• Term gestation?

• Clear amniotic fluid?•

Breathing or crying?

•

Good muscle tone?

•

Provide warmth1

• Position; clear airway (as

necessary); clear mouth

and nose of secretions2

•

Dry, stimulate3, reposition

•

Evaluate respirations,

heart rate, and color

•

Give

supplemental

oxygen5

•

Provide positive-pressure ventilation6

• Provide positive-pressure ventilation

•

Administer chest compressions7

•

Administer epinephrine8

• Endotracheal intubation9 may become necessary if

positive-pressure delivery by mask is not helpful

Recheck effectiveness:•

Ventilation

• Chest compressions

• Endotracheal intubation

•

Epinephrine dlievery

• Consider possibility ofHYPOVOLEMIA10

Consider:•

Airway malformations

• Lung problems:

! Pneumothorax11

! Diaphragmatic

hernia12 • Congenital heart

disease

Consider discontinuing resuscitation

Yes Routine care:•

Provide warmth

• Clear airway

•

Dry

•

Assess color

For meconium stained

depressed infants4 • Do direct mouth

and tracheal

suctioning

3 0

s

3 0

s

3 0

s

HR


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•

Discontinue once,

! Heart rate is > 100 bpm

! Infant is breathing spontaneously

! Improvement in color and tone•

Continue if Heart rate is < 100 bpm

• Initiate chest compressions if Heart rate remains < 60 bpm

and perform intubation

7. Chest compressions

•

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

effective PPV

• Guidelines:

!

Deliver over lower 1/3 of sternum, depth of 1/3 theAP diameter of the chest cavity

! 3:1 compression to ventilation ratio every 2 seconds

(90 compressions and 30 ventilations/minute)

! Every 30 seconds re-evaluate respiratory effort, color,

pulse, muscle tone

•

Two finger technique

! Two fingers (middle and ring) are used to deliver

compression while the other hand supports the back•

Two thumb circling hand technique

! More effective: higher peak systolic and coronary

perfusion pressure

! Two thumbs deliver the compression with provider’s

hands encircling infant and supporting the back

• Discontinue if Heart rate is > 60 bpm

8.

Epinephrine

•

Indications:! Asystole

! Bradycardia (Heart rate < 60 seconds after 30

seconds of effective PPV with 100% oxygen and

chest compressions)

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

mg/kg) per dose of 1:10000 solution

! Higher doses are NOT recommended from studiesshowing:

(1) Exaggerated hypertension

(2)

Decreased myocardial function

(3) Worse neurologic function (dose 0.1 mg/kg)

•

Recommended ET tube dose while IV access is being

obtained: 0.3 to 1 ml/kg

•

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

patient carefully between doses9.

Endotracheal intubation

•

Indications:

! Poor response to/inability to provide adequate PPV

! Need for endotracheal suctioning or chest

compressions

! Extreme prematurity

! Suspected diaphragmatic hernia•

Successful intubation is evidenced by bilateral chest rise

and improvement of heart rate, color, and muscle tone

•

IF ET tube is advanced too far, maintstem bronchus

intubation occurs and breath sounds are diminished over

half of the chest, withdraw tube slowly until equal bilateral

breath sounds are auscultated

• Formula for depth of intubation:

! Depth in cm = 6 + infant’s weight (in kg)•

Monitor oxygen saturation and evidence ofpneumothorax

10. HYPOVOLEMIA

•

Clinical manifestations:

! Pallor

! Weak pulses

! Delayed capillary refill! Persistent bradycardia

! Failure to respond to well-administered resuscitation

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

Normal Saline Solution

• Follow with packed RBCs if there is large volume blood

loss or poor response to crystalloid

11.

PNEUMOTHORAX

• Can rapidly lead to Tension Pneumothorax and

potentially lethal cardiorespiratory compromise

• Risk factors:

! Prematurity

! Meconium aspiration syndrome

•


! Tachypnea

! Retractions

! Grunting

! Tachycardia

!

*Bradycardia with symptoms of shock in TensionPneumothorax

•

If significant respiratory distress is present perform needle

decompression using a 20 gauge needle placed into the

affected lung either in:

! 4th ICS AAL

! 2nd ICS MCL

12. DIAPHRAGMATIC HERNIA

•

Defect in the diaphragm, usually on the left side, gives riseto displacement of the lung by abdominal content

entering the chest cavity

•


! Respiratory distress

! Cyanosis

! Scaphoid abdomen

•

Place gastric tube to decompress stomach, administe

oxygen•

Intubate and start PPV

! AVOID bag-mask ventilation as this will lead to

gastric distention and further respiratory compromise

References 1. Perinatal Asphyxia by Dr. Emilio A. Hernandez from the Handbook o

Medical and Surgical Emergencies, 6th ed, published by Elsevier 2007

2. USMLE Roadmap: Biochemistry by Richard G. Macdonald and William

G. Chaney, published by Lange 2007

3. Pediatric Emergency Medicine, 3rd edition, Gary R. Strange et al4. Guidelines on Basic Newborn Resuscitation by the World Health

Organization 2012

5.

Perinatal Asphyxia by William McGuire from the British Medical Journa

published on March 2007

6. Pathophysiology of perinatal asphyxia: can we predict and improveindividual outcomes? By Paola Morales, et al from the Official Journa

of the European Association for Predictive, Preventive, andPersonalized Medicine published on June 2011

7. Textbook of Neonatal Resuscitation, 5th edition, American Academy oPediatrics and American Heart Association


4/24

8 DIARRHEAL DISEASES AND DEHYDRATION

Definitions

•

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

period, with the more important feature being the consistencyrather than the number of stools. Best described as excessive

loss of fluid and electrolyte in the stool.

! Acute – lasting for a few hours or days

! Chronic (persistent) – lasting for 2 weeks or longer

•

Dysentery – small-volume, frequent bloody stools with mucus,

tenesmus, and urgency

• Dehydration

!

Loss of fluid without loss of supporting tissues! Contraction of extracellular volume in relation to cell mass

! Most common disturbance of water balance in pediatrics

! May result from:

1.

External loss of water and salt

2. External loss of salt without water deficit

3.

External loss of water alone

Epidemiology (1993 Statistics from the Health Intelligence Service)•

Leading cause of morbidity and 9th leading cause of mortality

for all ages

•

4th leading cause of death among infants in the Philippines

• Mortality due to delayed replacement of fluid and electrolyte

losses, and starvation leading to acute dehydration and

malnutrition

Common Etiologic AgentsVIRUSES BACTERIA PARASITES

Rotavirus

Norwalkagent

Adenovirus

CalicovirusCoronavirus

Astrovirus

Escherichia coli

(Enterotoxigenic, Enteropathogenic,Enteroinvasive, Enterohemorrhagic,

Enteroadherent)

VibriocholeraeShigella

Campylobacter jejuni

Staphyloccocus aureusClostridium difficile

Clostridium perfringens

Yersinia enterocoliticaVibrio parahaemolytica

Aeromonas hydrophila

Bacillus cereus

Entamoeba histolytica

Giardia lambliaStrongyloides

Trichuris trichuria

Cryptosporidia

Common Differential DiagnosesINFANT CHILD ADOLESCENT

AcuteGastroenteritisSystemic infection

Antibiotic associated

Gastroenteritis

Food poisoningSystemic infection


GastroenteritisFood poisoning


Chronic

Postinfectioussecondary lactase

deficiency

Cow’s milk/soy proteinintolerance

Chronic nonspecific

diarrheaCeliac disease

Cystic fibrosisAIDS enteropathy

Postinfectioussecondary lactase

deficiency

Irritable bowel syndromeCeliac disease

Lactose intolerance

GiardiasisInflammatory bowel

diseaseAIDS enteropathy

Irritable bowel

syndrome

Inflammatory boweldisease

Lactose intolerance

GiardiasisLaxative abuse

(Anorexia nervosa)

Pathophysiology Mechanism SECRETORY OSMOTIC

Cause Secretagogue (e.g. Cholera toxin)binds to receptor on the surface of the

epithelium of the bowel to stimulate

intracellular accumulation of cAMP orcGMP leading to excessive secretion

with decreased absorption

Ingestion of poorly absorbedsolute which is fermented in

the colon producing Short

Chain Fatty Acids, increasingosmotic solute load

StoolExamination

Watery, normal osmolality Watery, acidic, (+) reducingsubstances, increased

osmolality

Examples Cholera, Toxigenic E. coli, carcinoidsyndrome, VIP, neuroblastoma,

congenital chloride diarrhea,

Clostridium difficile cryptosporidiosis (AIDS)

Lactase deficiency, glucose-galactose malabsorption,

lactulose, laxative abuse

Effect of

fasting

Persists during fasting Stops with fasting

Mechanism INCREASED INTESTINAL MOTILITY DECREASED INTESTINAL MOTILITY

Cause Decreased transit time Defect in neuromuscular unit(s)or Stasis due to bacterial

overgrowth

Stool

Examination

Loose to normal-appearing stool,

stimulated by gastrocolic reflex

Loose to normal-appearing stoo

Examples Irritable bowel syndrome,

thyrotoxicosis, postvagotomy

dumping syndrome

Pseudo-obstruction, blind loop

Effect of

infection

Infection may contribute to

increased motility

Possible bacterial overgrowth

present

Mechanism MUCOSAL INFLAMMATION

Cause Inflammation, decreased mucosal surface area and/or colonic

reabsorption, increased motility

StoolExamination

Blood and increased WBCs in stool

Examples Celiac disease, Salmonella, Shigella, Amebiasis, Yersinia,

Campylobacter, Rotavirus, enteritis

Evaluation

ASSESS HYDRATION STATUSGROUP A GROUP B GROUP C

General

conditionWell, alert Restless, irritable

Lethargic,

unconscious, floppy

Eyes Normal Sunken Very sunken and dry

Tears Present Absent Absent

Mouth and

tongueMoist Dry Very dry

ThirstNot thirsty, drinks

normallyThirsty, drinks eagerly

Drinks poorly or notable to drink

Skin pinchGoes back quickly

< 2 seconds

Goes back slowly

> 2 seconds

Goes back very

slowly

> 3 secondsStatus NO DEHYDRATION SOME DEHYDRATION SEVERE DEHYDRATION

Management PLAN A: TREAT DIARRHEA AT HOME

Indications:

1. Children with no dehydration

2.

Improved status after Plan B or C

3. Children that cannot be returned to the health worker i

diarrhea gets worse

Goals:

1.

Treat child’s current episode of diarrhea at home2. Give early treatment for future episodes of diarrhea

Three rules for treating diarrhea at home:

1. Give the child more fluids than usual to prevent dehydration

•

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

possible, give plain water.

•

Give as much of these fluids as the child will take.• Continue giving these fluids until the diarrhea stops• Instructions: Dissolve 1 packet of ORS solution in 200 ml o

water and give as follows,

AGE AMOUNT AFTER EACH LOOSE STOOL MAINTENANCEA

< 24 months 50 – 100 mL 500 mL/day

2 – 10 years 100 – 200 mL 1000 mL/day

> 10 years As much as wanted 2000 mL/day

•

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

• For older, give frequent sips from a cup• If child vomits, wait for 10 minutes then give solution more

slowly thereafter

• Give ORS packets enough for 2 days of treatment

PLAN A PLAN B PLAN C

Persistent

vomiting orrefuses to

drink

If improved,

revert to Plan

A or Plan B

Patient improves Patient worsens

NGT


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2.

Give the child plenty of food to prevent under nutrition

• Continue to breastfeed frequently

•

If not breastfed, give usual milk

• If < 6 months old and not yet taking solid food, dilute milk

formula with equal amount of water for 2 days

• If > 6 months or already taking solid food,

! Give cereal or other starchy food mixed with

vegetables, meat, or fish. Add 1 to 2 teaspoonfuls of

vegetable oil to each serving

! Give fresh fruit juice or mashed bananas to provide

Potassium

!

Give freshly prepared food. Cook and mash or grindfood well

! Encourage child to eat, offer at least 6 times daily

! Give same foods after diarrhea stops, give extra

meal each day for 2 weeks

3. Take child to health worker if child does not get better in 3

days or develops any of the following:

• Many watery stools

•

Repeated vomiting•

Marked thirst

• Eating or drinking poorly

•

Fever

• Blood in stool

PLAN B: TREATMENT OF SOME DEHYDRATION

1.

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

•

If weight is unknown,Age < 4 mon 1 – 11 mon 12 – 23 mon 2 – 4 yrs 5 – 14 yrs > 15 yrs

Wt < 5 kg 5 – 7.9 kg 8 – 10 kg 11 – 15.9 kg 16 – 29.9 kg > 30 kg

mL 200 – 400 400 – 600 600 – 800 800 – 1200 1200 – 2200 > 2300

•

If weight is known,! Approximate ORS to be given by:

Weight in kg x 0.75 mL

• If the child wants more ORS, give more

•

Encourage mother to continue breastfeeding

• For infants < 6 months who are not breast fed, also give

100 – 200 ml clean water during this period

2. Observe the child carefully and help the mother give ORS

•

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

For older, give frequent sips from a cup

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

slowly thereafter

•

If the child’s eyelids become puffy, stop ORS and giveplain water or breast milk then give ORS according to

plan A when puffiness is gone

3.

After 4 hours, reassess the child

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

asleep! Plan A

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

juice as in Plan A

• Signs of severe dehydration ! Plan C

4. If mother must leave before completing Plan B

•

Instruct how much ORS to finish in 4-hour treatment

• Give ORS packets enough for rehydration and 2 days

PLAN C: TREATMENT OF SEVERE DEHYDRATION Can you give

intravenous (IV)fluids

immediately?

Yes • If patient can drink give ORS PO while setting up

•

Start IVF immediately: 100 mL/kg Ringer’s LactateSolution or NSS as follows,

AGEFirst give

30 mL/kgThen give 70 mL/kg

< 12 mon 1 hour 5 hours

Older 30 mins 2.5 hours

• Repeat once if radial pulse is still very weak or not

detectable

• Reassess the patient every 1 – 2 hours. If hydration is

not improving, give IV drip more rapidly•

As soon as patient can drink give ORS (5 mL/kg/hr)

usually after 3 – 4 hours (infants) or 1 – 2 hours (older)

•

After 6 hours (infants) or 3 hours (older) re-evaluate

hydration status and treat accordingly

No

Is IV treatmentavailable nearby

(within 30 mins)?

Yes • Send patient immediately for IV treatment

• If patient can drink provide mother with ORS and

show her how to give it during the trip

No

Are you trained touse a nasogastric

tube for

rehydration?

OR

Can the patient

drink?

Yes • Start rehydration by tube/PO with ORS: Give 20mL/kg/hr for 6 hours (total of 120 mL/kg)

•

Reassess the patient every 1 – 2 hours

! Repeated vomiting or increasing abdominaldistension! Give fluid more slowly

! If hydration not improved in 3 hours! IVF

• After 6 hours, reassess and choose appropriatetreatment plan

No

URGENT: Send thepatient for IVF or

NGT treatment

• If possible, observe the patient at least 6 hours afte

rehydration to be sure mother can maintain hydration giving

ORS by mouth

• If patient is > 2 years old and there is cholera in your area, give

appropriate oral antibiotic when patient is alert

MANAGEMENT OF ASSOCIATED PROBLEMS

1. Blood in the stool •

Treat for 5 days with an oral antibiotic recommended fo

Shigella in your area: Trimethoprim (TMP) +

Sulfamethoxazole (SMX)

!

Children: TMP 5 mg/kg + SMX 25 mg/kg BID for 5 days! Adults: TMP 160 mg + SMX 800 mg BID for 5 days

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

• See the child again after 2 days if:

! < 1 years old! Initially dehydrated

! There is still blood in the stool

! No improvement

•

If the stools is still bloody after 2 days change ora

antibiotic to alternative recommended for Shigella in you

area,

(1) Nalidixic Acid ! Children: 15 mg/kg QID for 5 days

! Adults: 1 g TID for 5 days

(2) Ampicillin

! Children: 25 mg/kg QID

2.

Persistent diarrhea (> 14 days) •

Refer to the hospital if:

! < 6 months old

! Dehydration is present (treat first then refer)• Otherwise, teach mother to use Plan A, except:

! Dilute any animal milk with equal volume of water o

replace with fermented milk product such as yoghurt

! Assure full RENI by giving 6 meals a day, thick cerea

and added oil, mixed vegetables, meat, fish

•

Follow up in 5 days

! Diarrhea has not stopped! Refer to hospital

! Diarrhea has stopped:(1)

Use same food for regular diet

(2) After 1 week gradually resume usual milk

3

Give extra meal each da for at least 1 month


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3.

Severe undernutrition

• Do not attempt rehydration

•

Refer to hospital for management

• Give ORS 5 mL/kg/hr

4.

Fever

• Give Paracetamol q4 for Temperature 39.0°C or greater

•

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

fever of 38.0°C and above OR history of fever in the past 5

days: Give antimalarial

Other Common Antimicrobials for Diarrhea CAUSE ANTIBIOTIC OF CHOICE ALTERNATIVE(S)

Cholera Tetracycline

Children: 12.5 mg/kg QID for 3

daysAdults: 500 mg QID for 3 days

Or

Doxycycline

Adults: 300 mg OD for 3 days

Furazolidone

Children: 1.25 mg/kg QID for 3 days

Adults: 100 mg QID for 3 days

Or

Trimethoprim (TMP)

Sulfamethoxazole (SMX)

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

Adults: TMP 160 mg + SMX 800 mg

BID for 3 days

Amoebiasis Metronidazole

Children: 10 mg/kg TID for 5 days

Adults: 750 mg TID for 5 days

Severe cases:

Dehydroemetine hydrochloride

IM OD for 10 daysPO 1 – 1.5 mg/kg OD for 5 days

Giardiasis Metronidazole

Children: 5 mg/kg TID for 5 daysAdults: 250 mg TID for 5 days

Quinacrine HCl

Children: 2.5 mg/kg TID for 5 daysAdults: 100 mg TID OD for 5 days

References 1. Dr. Enrique H. Carandang’s Diarrheal Diseases and Dehydration from

the Handbook of Medical and Surgical Emergencies, 5 th edition2. Nelson Textbook of Pediatrics, 19th edition


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13 HEPATIC ENCEPHALOPATHY

Definition

• State of disordered CNS function resulting from failure of the

liver to detoxify noxious agents of gut origin because of

hepatocellular dysfunction and portosystemic shunting

(Current Medical Diagnosis and Treatment 2014) secondary to

a chronic hepatic pathology or acute hepatic failure

•

Syndrome of acute hepatic failure manifested as psyhicatric

and neurologic abnormalities with jaundice within 2 to 8 weeks

of onset of symptoms without pre-existing liver disease

(Handbook of Medical and Surgical Emergencies, 5th

edition)

Etiology

• Viral (Hepatitis)

•

Drugs – diuretics, opioids, hypnotics, sedatives

• Chemical – Ammonia: most readily identified and measurable

toxin, but is not solely responsible for disturbed mental status

• Others – surgery, radiation, cancer

Precipitating factors

• Azotemia

•

Electrolyte imbalance – hypokalemia, alkalosis

• High protein diet

•

Gastrointestinal bleeding

• Hypovolemia

•

Sedative/tranquilizer

•

Surgery

Pathogenesis

•

Normally, ammonia is produced from the breakdown of

dietary amino acids by colonic bacterial flora.

! Ammonia is reabsorbed by the portosystemic circulation.

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

the liver where it is converted into Urea.! Urea is released into the circulation and excreted in urine.

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

heart, and brain.

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

portosystemic shunting is present, there is failure of ammonia

detoxification into urea.

! Ammonia levels escalate but the ability of the kidneys,

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

•

Ammonia has multiple neurotoxic effects:

! Alters transit of amino acids, water, electrolytes across

astrocytes and neurons

! Impairs amino acid metabolism and energy utilization in

the brain

! Inhibits generation of excitatory and inhibitorypostsynaptic potentials

Manifestations

• Major features:

! Altered consciousness

! Personality change

! Motor abnormalities

! Neuro-ophthalmologic changes

! Electroencephalographic changes: slow, high-amplitude,triphasic waves

• West Haven Classification System

GRADE SYMPTOMS MOTOR EEG

0 Undetectable changes in personality, behavior(+) Minimal changes in memory, concentration,

intellect, coordination

(-) Normal

I Sleep reversal pattern, hypersomnia, or insomnia

Euphoria, depression, irritabilityMild confusion, slowed ability to do mental tasks

Tremors Normal

II Lethargy, drowsiness

Inappropriate behaviorDisorientation, gross deficits in ability to perform

mental tasks

Asterixis (+)

III SomnolenceAggressive behavior

Severe confusion, unable to perform mental

tasks, amnesia

Asterixis (+)

Diagnosis

• Usually clinical – characteristic signs, symptoms

Treatment: Reduce ammonia formation

1.

Nonabsorbable dissacharides

• Lactulose

! Mechanism of action:

(1) !igested by colonic bacteria to short-chain fatty

acids resulting to acidification of colon contents

! Acidification favors formation of Ammonium

ion (NH4+)which is not absorbable and nontoxic

(2)

Also leads to change in bowel flora to decreaseammonia forming organisms

(3)

Catharsis eliminates nitrogenous waste products

! Dose:

(1)

30 ml PO tid-qid with maintenance dose

adjusted to produce 3 to 5 soft stools per day

(2)

If patient cannot tolerate PO give Lactulose 300

ml added to 700 ml distilled water as retention

enema for 30 to 60 minutes qid to q6h2.

Antibiotics: to control ammonia producing intestinal flora

• Alternating administration of:

(1)

Neomycin 500 – 1000 mg q6h PO

! Interferes with bacterial protein synthesis by

binding to 30S ribosomal subunit

! Adverse effects: ototoxicity, nephrotoxicity

(2)

Metronidazole 250 mg q8h PO

! Adverse effect: peripheral neuropathy

! Inhibits nucleic acid synthesis by disrupting DNA

• Alternative:

(3)

Rifaximin 550 mg BID PO

! Binds to !-subunit of bacterial DNA dependen

RNA polymerase

! Better safety profile

3. Control GI bleeding and purge blood from the GIT•

Magnesium citrate 120 ml PO

• Nasogastric tube every 3 – 4 hours

4.

Diet

• Dietary protein restriction

! No longer recommended by current studies because

malnutrition outweighs the benefits of restriction

! Most patients found to be able to tolerate high

protein diets

! For those unable to tolerate protein shift to

vegetable sources of protein

Supportive measures

1. Fluid/electrolyte replacements

2.

Oxygen inhalation

3. Monitor urinary output, CVP, vital signs

Complications

•

Coagulation defect, leading to bleeding

• Predisposed to infections

• Respiratory defects, leading to hypoxemia

• Hypovolemia leading to tubular necrosis then renal failure

• Cerebral edema leading to encephalopathy

References 1. Handbook of Medical and Surgical Emergencies, 5 th edition

2. The Washington Manual of Medical Therapeutics 33rd edition

3. Current Diagnosis and Treatment: Emergency Medicine, 6 th edition


8/24

14 HYPERTENSIVE URGENCIES AND EMERGENCIES

Definitions

•

Hypertension – presence of blood pressure (BP) elevation to a

level that places patients at increased risk for target organdamage in several vascular beds including the retina, brain,

heart, kidneys, and large conduit arteriesSBP DBP

Normal BP < 120 mmHg < 80 mmHg

Prehypertension 120 – 139 mmHg 80 – 89 mmHg

Stage 1 140 – 159 mmHg 90 – 99 mmHg

Stage 2 > 160 mmmHg > 100 mmHg

• Hypertensive Crisis

! Includes hypertensive urgencies and emergencies

! Usually develops in patients with previous history of

elevated BP but may arise in previously normotensive

! Severity correlates with absolute level of BP elevation and

rapidity of development (autoregulatory mechanisms

have not had sufficient time to adapt)URGENCY EMERGENCY

Definition Severely elevated BP

(DBP > 120 mmHg) in

a patient with nosymptoms, signs, or

laboratory findings of

end-organ damage

Severely elevated blood pressure (SBP > 210

mmHg and DBP > 130 mmHg) responsible for

symptoms, signs, or laboratory evidence ofend-organ damage

Accelerated HTN – SBP > 210 mmHg and DBP> 130 mmHg with headaches, blurred vision,

or focal neurologic symptoms

Malignant HTN – accelerated HTP with

papilledema

Precipitating settings Optic disk edemaSevere perioperative

hypertension

Rebound from abruptcessation of

adrenergic inhibiting

drugs

Hypertensive encephalopathyIntracerebral Hemorrhage

Unstable Angina Pectoris

Acute Myocardial InfarctionAcute LV failure with pulmonary edema

Dissecting aortic aneurysm

Progressive renal failure

Eclampsia

•

Determinants of arterial pressure

Etiology

• 90% of patients have Primary or Essential Hypertension

• 10% of patients have Secondary Hypertension! Renal parenchymal disease

! Renovascular disease

! Pheochromocytoma

! Cushing’s Syndrome

! Primary Hyperaldosteronism

! Coarctation of the aorta

! Obstructive sleep apnea

Management

Laboratories and ancillaries to identify patients with possible targetorgan damage – assess cardiovascular risk and provide baseline

for monitoring adverse effects of therapy

1.

Urinalysis

2. Hematocrit

3.

Plasma glucose4. Serum potassium

5.

Serum creatinine

6. Calcium

7.

Uric Acid

8. Fasting lipid levels

9. Electrocardiogram

10. Chest X-ray

11. Echocardiography

Treatment URGENCY EMERGENCY

BP reduction Within 24 hours Reduction of 20 to 25% in MAP [(2 DBP +SBP)/3] within 1 hour to prevent or minimize

end-organ damage

Avoid rapid, severe drops in BP because

Watershed Cerebral Infarction can occur

If possible, admit to Intensive Care Unit and

consider placing an Intra-arterial line for

constant BP monitoring

Anti-

hypertensive

agents

Clonidine 0.2 mg PO

followed by 0.1 mg

every hour until BP is

controlledCaptopril 12.5 – 25

mg PO or

Labetalol 200 – 400

mg PO

Nitroprusside – potent vasolidator

Lowers BP in seconds

Insert intra-arterial line to ensure over titration

leading to hypoperfusion does not occurContinuous IVI 0.5 – 10 "g/kg/min

Nitroglycerin – for situations whereinNitroprusside is relatively contraindicated (i.e

Severe coronary insufficiency, advanced

renal or hepatic disease)

Labetalol – combination # and ! blocker

IV bolus 20-80 mg over 2 minutes q5-10mMay be doubled every 10 minutes until BP

reduction achieved

Max total dose of 300 mg

Hydralazine – vasodilator that may be used

in pregnancy since it also increases uterine

blood flowIV 10 – 20 mg every 15 – 30 mins

Continuous IVI 1.5 – 5.0 "g/kg/min

Fenoldopam – dopaminergic agonist usefulin renal insufficiency or failure as alternative

to Nitroprusside (Cyanide toxicity)

Continuous IVI 0.1 – 0.3 "g/kg/minEnalaprilat – IV ACEI useful for congestive

heart failure, stroke, as alternative to

Nitroprusside0.6255 mg/dose over 5 mins q6h

Phentolamine – alpha-adrenergic receptor

blocker useful in Pheochromocytoma crisisContinuous IVI 50 – 300 "g/kg/min

Diazoxide – potassium channel activator tharelaxes smooth muscles to decrease PVR,

increase HR and CO, useful for renal failure

IV bolus 20 – 80 mg q5-10 mins

Nicardipine – CCB useful in post-op HTN

Nifedipine – CCB useful in angina

• Furosemide – loop diuretic which blocks sodium reabsorption

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

References 1. Dr. Adoracion Nambayan-Abad’s Hypertensive Crises: Emergencie

and Urgencies from the Handbook of Medical and Surgica

Emergencies, 5th edition2. The Washington Manual of Medical Therapeutics 33rd edition

3. Current Diagnosis and Treatment: Emergency Medicine, 6 th edition

4.

Acute Care Evaluation and Management of Hypertensive Emergencie

Emergency Medicine Cardiac Research and Educational GroupInternational

Arterialpressure

Cardiacoutput

Strokevolume

Heart rate

Peripheral

resistance

Vascularstructure

Vascularfunction


9/24


10/24

20 HEMOPTYSIS

Definition[1,2]

• Expectoration of the blood from the lungs or bronchial tubes

or coughing out blood in gross amounts or fine streaks from a

source below the glottis (Steadman’s Medical Dictionary)

•

Massive hemoptysis

! Occurs in 5% of cases

! 200 to 600 mL of blood expectorated in 24 hours

! Clinically, any bleeding that results in the impairment of

lung function and gas exchange

!

Originates from a bronchial artery in 90% of cases! 20% fatality rate

Causes[1] 1. Infections

1.1. Bronchiectasis

1.2. Acute/chronic bronchitis1.3. Necrotizing pneumonias

1.4.

Pulmonary Tuberculosis – fever and night sweats

1.5. Lung abscess

1.6. Fungal infections (Aspergilloma)1.7. Amoebic liver abscess (Pleuro-pneumonic complications)

1.8.

Paragonimiasis

2. Neoplasms – weight loss and change in cough

2.1. Primary2.1.1. Bronchial adenoma

2.1.2. Carcinoid tumor

2.1.3. Bronchial cancer

2.2.

Metastatic2.2.1. Choriocarcinoma

2.2.2. Osteogenic carcinoma

3. Cardiovascular conditions

3.1. Mitral stenosis – chronic dyspnea and minor hemoptysis3.2.

Acute pulmonary edema

3.3. Aortic aneurysm rupture in a bronchus

3.4. Atrioventricular malformations

4.

Thromboembolic – dyspnea and pleuritic chest pain

Pulmonary infarction from:4.1. Deep Venous Thrombosis

4.2. Septic emboli

4.3.

Fat embolism

5. Trauma5.1. Blunt/crushing injuries/pulmonary contusion

5.2. Penetrating injuries from rib fractures

5.3. Bullet or bladed weapons

6. Iatrogenic 6.1.

Related to maintenance of airway patency (endotracheal and

tracheostomy tubes – both tip and balloon related)

6.2. Related to hemodynamic monitoring of the critically ill –

pulmonary catheter related via:6.2.1. Perforation/rupture

6.2.2.

Pulmonary infarction

6.3. Related to diagnostic procedures:

6.3.1. Bronchoscopy with biopsy (transbronchial biopsy,transbronchial lung biopsy)

6.3.2.

Percutaneous lung biopsy

7. Massive Hemoptysis in the ICU

7.1. Hemoptysis complicating a systemic disease7.2. Hemoptysis complicating a therapeutic or diagnostic procedure

7.3. Trauma from vigorous suctioning

8. Miscellaneous

8.1. Anticoagulation

8.2. Thrombocytopenia

8.3.

Disseminated Intravascular Coagulation8.4. Aspiration (Foreign bodies, gastric content)

8.5. Blood dyscrasias

8.6. Auto-immune diseases: Good Pasture’s Syndrome, SLE, Wegener’granulomatosis)

8.7. Idiopathic (Pulmonary hemosiderosis)

9.

Cryptogenic Hemoptysis

9.1. Found in 20% of cases9.2. Undetermined cause despite extensive evaluation

(bronchoscopy, CT scan, bronchogram)

Clinical Manifestations[1]

•

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

hemorrhage

•

True hemoptysis vs. Epistaxis

! True hemoptysis

1.

Bleeding below the glottis

2. Follows coughing spells! Epistaxis

1. Bleeding above the glottis (upper airway source)

2.

Sensation of pooling of blood in the throat or need to

clear the throat before bleeding

•

Minor hemoptysis or blood-streaked sputum

! With/without discomfort/bubbling sensation over chest

! If with repeated episodes consider massive hemorrhage

•

Massive hemoptysis! Asphyxiation from flooding of the airways resulting to

acute respiratory failure

1. Tachypnea

2.

Dyspnea

3. Audible rhonchi

4.

Cyanosis

! Hemodynamic alterations from acute blood loss

1.

Pallor2.

Dizziness

3. Hypotension

Diagnosis[1]

•

Goals

! Determine site, cause, degree of hemorrhage

! Assess hemodynamic, ventilator, and oxygenation status

! Determine need, feasibility, application of appropriatemedical and surgical interventions

• Work-up

! History and PE may suggest etiology

! ENT examination to rule out upper airway source o

bleeding

1. Rhinoscopy

2. Nasopharyngeal and laryngeal endoscopy! Chest X-ray to determine site, etiology, extent of disease

! CBC with platelet and coagulation studies

! Gross, bacteriologic cytologic examinations of sputum

(character, appropriate smears/cultures, and

cytopathology)

! Arterial blood gas: assess oxygenation, ventilator, and

acid-base status

! Bronchoscopy : can be both diagnostic and therapeutic1.

Fiber-bronchoscope for mild or moderate bleeding

2.

Rigid scope for massive bleeding – better visibility

suctioning, airway control

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

bronchial/pulmonary lesions or interstitial lung diseases

Treatment [1] •

Existing clinical practice guidelines are disease specific

Management of MILD HEMOPTYSIS

Mild hemoptysis

Disease specific treatment

Fiber bronchoscopy Tx: Medical/Surgical

CT scan or Bronchography Tx: Medical/Surgical

Conservative treatment

} Acute fever, cough, bloody sputum

} Indolent productive cough

5. Changes in sensorium

6.

Coma

7. Death

4. Rapid pulse

5.

Cold clammy skin

Bed rest

Antitussives

Chest X-ray

(CT scan if indicated)

Positive

Negative

Positive

Negative

Persistent bleeding


11/24

Minor Hemoptysis

• No specific intervention required for small amounts of blood in

the sputum other than that directed toward primary disease

and watchful waiting•

Non-pharmacologic:

! Avoid strenuous/competitive activities

! Stop any anticoagulants and anti-platelets

! Avoid chest percussion or vigorous physiotherapy

! May be initially controlled during diagnostic

bronchoscopy

• Pharmacologic:

!

Disease specific treatment ASAP! Cough suppressants: optional, use with caution

Examples[3]

1. Dextromethorphan – levorphanol derivative, has

central action on the cough center in the medulla

2. Codeine – phenantrene-derivative opiate agonist

that binds to opiate receptors in the CNS to cause

analgesia, has central action on the cough center in

the medulla3.

Benzonatate – non-narcotic antitussive with local

anesthetic effect on stretch receptors in respiratory

passages and lungs that reduces cough reflex

Management of MASSIVE HEMOPTYSIS (200 – 600 ml/24 hours)

MASSIVE HEMOPTYSIS

• Real danger in massive hemoptysis is asphyxia not blood loss

•

Monitor/maintain airway patency and adequacy o

ventilation! Patient in head down position with bleeding side

dependent to avert aspiration into the opposite lung

! Intubate, oxygenate, mechanically ventilate fo

impending respiratory failure

•

Initial volume resuscitation

! Crystalloid or colloid infusions initially

! Whole blood transfusions for recurrent moderate to severe

bleeding• Localize, isolate, and arrest the hemorrhage

! Bronchoscopy (rigid) to visualize and pack bleeding site

! Appropriate use of Fogarty embolectomy catheter fo

balloon occlusion

! Use of Carlens double lumen tube allows isolation and

separate ventilation of each lung

! Resectional surgery for localized disease with recurren

massive bleeding and failed medical treatment

! Selective arterial embolization for diffuse disease and fo

patients who refuse surgery

•

Initiate disease specific treatment

! Consider resectional surgery or selective arteria

embolization after tamponade in patients with > 400 ml o

expectorated blood in the first 3 hours or > 600 ml within

24 hours

References 1. Hemoptysis by Dr. Bernardo D. Briones, Handbook of Medical and

Surgical Emergencies

2. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide3.

MIMS Drug Information System Philippines

Massive hemoptysis

History, Physical Examination

Assess oxygenation/ventilation status

(Intubate/ventilate for impending respiratory failure)Assess hemodynamic status

(Crystalloids, Colloids, Blood)

Chest X-ray (CT scan may be indicated)

Bronchoscopy (rigid or fiberscope)

Source identified No identifiable source

Suction/lavage

Selective Endobronchial Intubation

Endobronchial Tamponade

Double Lumen Endotracheal Tube

Surgery

indicated

Surgery

contraindicatedor patient refuses

Bronchial

arteriography

Resectional

surgery

Arterial

embolization

Source identified No identifiable source

Pulmonaryarteriography

ICULie on side affected/Head

down position


12/24

26 THYROID STORM / THYROTOXIC CRISIS by: toxic JI

Essentials of Diagnosis

# Typical stigmata of hyperthyroidism, thyromegaly,ophthalmopathy, tremor, stare, diaphoresis, and agitation

# Fever (usually)

# Tachycardia (out of proportion to fever) often with associated

atrial arrhythmias

# Mental status changes ranging from confusion to coma

Introduction/Definition

# Thyroid hormone affects all organ systems and is responsiblefor increasing metabolic rate, heart rate, and ventricle

contractility, as well as muscle and central nervous system

excitability.

# Two major types of thyroid hormones are thyroxine and

triiodothyronine.

o Thyroxine is the major form of thyroid hormone.

o The ratio of thyroxine to triiodothyronine released in the

blood is 20:1.o

Peripherally, thyroxine is converted to the active

triiodothyronine, which is three to four times more potent

than thyroxine.

# Hyperthyroidism refers to excess circulating hormone resulting

only from thyroid gland hyperfunction, whereas thyrotoxicosis

refers to excess circulating thyroid hormone originating from

any cause (including thyroid hormone overdose).

#

Thyroid storm is the extreme manifestation of thyrotoxicosis. Thisis an acute, severe, life-threatening hypermetabolic state of

thyrotoxicosis caused either by excessive release of thyroid

hormones causing adrenergic hyperactivity or altered

peripheral response to thyroid hormone following the

presence of one or more precipitants.

# The mortality of thyroid storm without treatment is between

80% and 100%, and with treatment, it is between 15% and 50%.# In the case of thyroid storm, the most common underlying

cause of hyperthyroidism is Graves’ disease.

# It occurs most frequently in young women (10 times more

common in women compared with men) at any age

Causes

# MOST COMMON: Thyroid storm usually occurs when an

already thyrotoxic patient (Graves disease, toxic multinodulargoiter, and toxic adenoma are most common) suffers a serious

concurrent illness, event, or injury.

# During thyroid storm, precipitants such as infection, stress,

myocardial infarction, or trauma will multiply the effect of

thyroid hormones by freeing thyroid hormones from their

binding sites or increasing receptor sensitivity.

Clinical Manifestations

# The diagnosis of thyroid storm should be made clinically.

#

Often a history of partially treated hyperthyroidism or signs o

thyroid disease such as thyromegaly, proptosis, stare, myopathyor myxedema can be found.

# The diagnosis should be made in the patient with a probable

history of thyroid disease, which rapidly decompensates in the

setting of fever, tachycardia, gastrointestinal symptoms, and

mental status change.

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

state of thyrotoxicosis# Cardiac findings usually include a friction rub or systolic flow

murmur, and either sinus or supraventricular tachycardia. The

heart rate is often characterized as out of proportion to fever.

# Mental status changes are also common.

# Gastrointestinal symptoms include nausea, vomiting, diarrhea

and abdominal pain—can mimic an acute abdomen.

#

Neuromuscular findings such as agitation, tremor, generalizedweakness (especially in the proximal muscles), and periodic

paralysis are also seen.

# Dermatologic findings include warm, moist, smooth skin and

palmar erythema.

# Apathetic hyperthyroidism is important to consider in the

elderly population. With advanced age and other comorbid

conditions, the classic symptoms and signs of thyroid storm

and thyrotoxicosis may be absent.

Ancillary Diagnostic Findings

#

Draw blood samples to test for free T4, T3, and TSH (thyroid

stimulating hormone) and serum cortisol levels.

# A complete blood count, serum electrolytes, glucose rena

and hepatic function tests, and ABG analysis should be

performed;

# Obtain cultures of the blood, urine, and possibly sputum; chesX-ray and ECG are indicated to look for precipitating cause

or complications.

# Cranial CT scan is indicated for delirious or comatose patients.

# Previous abnormal thyroid function tests may suggest a

preexisting thyrotoxicosis. TFTs may be misinterpreted based on

levels of thyroid binding globulin.

# TSH will be markedly low in most patients with thyroid storm o

thyrotoxicosis. Free thyroxine (T4) will be elevated, again similato thyrotoxicosis.

# Electrolyte and glucose abnormalities may also be presen

due to gastrointestinal losses, dehydration, physiologic stress

and fever

# The ECG is usually abnormal; common findings are sinus

tachycardia, increased QRS interval and P wave voltage

nonspecific ST–T wave changes, and atrial dysrhythmiasusually atrial fibrillation or flutter


13/24

Emergency Measures

SHORCUT:

Treatment aims are as follows:

1. Supportive care2.

Inhibition of new hormone synthesis

3. Inhibition of thyroid hormone release

4.

Peripheral !-adrenergic receptor blockade

5. Preventing peripheral conversion of thyroxine to

triiodothyronine

6. Treat precipitating event

LONGCUT:1. Supportive care

# General: oxygen, cardiac monitoring Fever: external

cooling; acetaminophen 325–650 milligrams PO/PR every

4–6 h (aspirin is contraindicated because it may increase

free thyroid hormone)

# Volume replacement: is commonly indicated with at least

1 L of normal saline or lactated Ringer's solution in the first

hour due to volume depletion from fever.#

Nutrition: glucose, multivitamins, thiamine, including folate

can be considered (deficient secondary to

hypermetabolism)

# Cardiac decompensation (atrial fibrillation, congestive

heart failure): rate control and inotropic agent, diuretics,

sympatholytics as required

2.

Inhibition of new thyroid hormone synthesis with thionamides # Thionamides are the standard first-line agents to treat

thyroid storm.

# Methimazole. (Avoid methimazole for pregnant women

in first trimester as it can cause teratogenic effect. It can

only be used in second and third trimester of pregnancy.)

# PTU, (PTU also blocks peripheral conversion of thyroxin to

triiodothyronine.) (PTU is used for pregnant women in firsttrimester. PTU also has a boxed warning issued by the U.S.

Food and Drug Administration in 2010 regarding its rare

but severe side effect toward liver function.

# Methimazole is preferred as first-line treatment unless

contraindicated.)

3.

Inhibition of thyroid hormone release

(at least 1 h after step 2) #

Iodine therapy is an adjunct to the thionamides.

#

It should not be given until at least 1–2 hours after PTU or

methimazole is administered. Early administration can

promote further hormone production, thus worsening

hyperthyroidism.

#

Several forms are available such as potassium iodide (SSKI,

35 mg/drop) 5 drops PO every 6 hours or Lugol's solution 8drops every 6 hours.

# If iodine allergy is a concern, lithium carbonate can be

given instead

4. !-Adrenergic receptor blockade

# ! -Adrenergic agonists such as propranolol block the

peripheral effects of excess thyroid hormone.

# Beta blockers may be especially attractive in cases of

atrial fibrillation with rapid ventricular response

5. Preventing peripheral conversion of thyroxine to

triiodothyronine

# Corticosteroids inhibit peripheral conversion of T4 to T3

and block the release of hormone from the thyroid

gland.# In addition, they treat the relative adrenal insufficiency

that may be present

# Intravenous hydrocortisone, 100 mg every 8 hours, is the

treatment of choice for concurrent adrenal

insufficiency; however, dexamethasone, 0.1 mg/kg

intravenously every 8 hours, may be given

6.

Treat precipitating event

# All triggers of thyroid storm should be searched and

treated accordingly (infection, myocardial infarct

diabetic ketoacidosis, etc.).


14/24

29 ANIMAL BITES

•

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

on the hands or face•

If unprovoked, the bite is usually in the legs, thighs, or buttocks

• Dog bites tend to be crushing injuries or puncture wounds

rather than clean, sharp lacerations

• Complications:

! Wound infection or abscess

! Fractures

! Septicemia

RABIES

•

Rapidly progressive, acute infectious disease of the central

nervous system in humans and animals caused by infection

with the Rabies virus normally transmitted from animal vectors

• Rabies virus

! Family Rhabdoviridae

! Lyssavirus: causes serious neurologic disease when

transmitted to humans

! Vesiculovirus: causes vesiculation and ulceration in cattle,

horses, and other animals and causes self-limited, mild

systemic illness in humans

Pathogenesis

1. Incubation period (interval between exposure and onset of

clinical disease) – 20 to 90 days

2. During incubation, the virus is present or close to site of

inoculation3. In muscles, virus binds to nicotinic acetylcholine receptors on

postsynaptic membranes at neuromuscular junctions

4. Virus spreads centripetally along peripheral nerves toward

CNS at 250 mm/d via retrograde fast axonal transport to spinal

cord or brainstem

5.

Virus rapidly disseminates to other regions of CNS via fast

axonal transport along neuroanatomic connections

•

Neurons are prominently infected•

Babes nodules – microglial nodules

•

Negri body

! Most characteristic pathologic finding

! Eosinophilic cytoplasmic inclusions in brain neurons

composed of virus proteins and viral RNA! Common in Purkinje cells of Cerebellum and

Pyramidal neurons of Hippocampus

6.

Centrifugal spread along sensory and autonomic nerves to

other tissues including:

•

Salivary glands: virus replicates in acinar cells and

secreted in saliva

• Heart

•

Adrenal glands• Skin

Clinical manifestations

PhaseTypical

durationSymptoms and Signs

Incubation 20 – 90 d None

Prodrome 2 – 10 d Fever, malaise, anorexia, nausea, vomiting,paresthesias, pain, pruritus at wound site

Encephalitic

(80%)

2 – 7 d Anxiety, agitation, hyperactivity, bizarre

behavior, hallucinations, autonomic

dysfunction, hydrophobia

Paralytic(20%)

2 – 10 d Flaccid paralysis in limbs, progressing toquadriparesis with facial paralysis

Coma, death 0 – 14 d

Diagnosis

1.

Rabies virus specific antibodies – (+) serum neutralizingantibodies to rabies diagnostic in previously unimmunized butmay not develop until late in disease

2. RT-PCR amplification – highly sensitive and specific; saliva, CSF,

skin, brain tissue may be used

3. Direct fluorescent antibody testing – highly sensitive and

specific; can be performed quickly and applied to skin

biopsies and brain tissue

Prognosis • Almost uniformly fatal disease but always preventable with

appropriate postexposure therapy during early incubation

period

Treatment

• Guidelines

! Inquire about epidemiology of rabies in local community

! Unprovoked bites by wild or stray animals will always

require immunization with RIg and a complete course of


15/24

! Scratches by the claws of rabid animals are dangerous

because animals lick their claws. Saliva applied to a

mucosal surface may be infectious

! Also give Tetanus immunization depending on patient’simmunization status

SAN LAZARO HOSPITAL GUIDELINES

What are the guidelines for Rabies Post-Exposure Prophylaxis?

1. Apply local wound treatment immediately to exposures of all

types of category.

•

Vigorously wash and flush with soap or detergent andwater for 10 minutes

•

Apply alcohol, povidone iodine, or any antiseptic

• AVOID suturing

•

DO NOT apply ointment, cream, or dressing

• Apply antimicrobials (Co-amoxiclav, Cefuroxime axetil)

for the following conditions:

! Frankly infected wounds

! All category III bites•

Give Anti-Tetanus immunization if indicated

2. Assess the category of the wound and apply recommended

treatment.CATEGORY MANAGEMENT

CATEGORY I

• Feeding or touching an animal

•

Licking of intact skin

•

Exposure to patient with S/S of rabies by

sharing or eating or drinking utensils*•

Casual contact to patient with S/S of

rabies*

Local wound treatment

NO vaccine or RIG needed

*Consider Pre-exposure vaccination

CATEGORY II• Nibbling/nipping of uncovered skin with

bruising

•

Minor scratches/abrasions WITHOUTbleeding*

•

Licks on broken skin

•

*Include wounds that are INDUCED tobleed

Start vaccine immediately

1.

COMPLETE regimen until Day 28/30 if:

•

Animal is rabid, killed, died, orunavailable for 14 day

observation and examination

•

Animal under observation diedwithin 14 days, was IFAT positive,

or no IFAT testing was done, or

had signs of rabies2.

COMPLETE regimen until Day 7 if:

• Animal is alive and remains

healthy after 14 days observation•

Animal died within 14 days, was

IFAT negative, and without any

signs of rabies

CATEGORY III •

Transdermal bites or scratches

•

*Include puncture wounds, lacerations,avulsions

• Contamination of mucous membrane

with saliva (i.e. licks)

•

Exposure to rabies patient through bites,contamination of mucous membranes or

open skin lesions with body fluids (except

blood/feces)•

Handling of infected carcass or ingestion

of raw infected meat•

All Category II exposures on head and

neck area

Start vaccine and RIG immediately

1.

COMPLETE regimen until Day 28/30 if:

•

Animal is rabid, killed, died, or

unavailable for 14 dayobservation and examination

•

Animal under observation diedwithin 14 days, was IFAT positive,

or no IFAT testing was done, or

had signs of rabies

2. COMPLETE regimen until Day 7 if:

• Animal is alive and remainshealthy after 14 days observation

• Animal died within 14 days, was

IFAT negative, and without anysigns of rabies

ACTIVE IMMUNIZATION PRODUCTS

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

! Adults: deltoid area of each arm

! Infants: anterolateral aspect of the thigh

! NEVER in the gluteal area because absorption is

unpredictable• Types:

1.

Purified Vero Cell Rabies Vaccine (PVRV) [0.5 ml]

2. Purified Chick Embryo Cell Vaccine (PCECV) [1.0 ml]

•

Vaccination regimen:

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

D0!D3!D7!D14!D28/30! Abbreviated multisite schedule IM (2-1-1):

2 D0!1 D7!1 D21

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

2 D0!2 D3!2 D7!0 D14!2 D30

•

Previously immunized animal bite patientsINTERVAL FROM LAST DOSE VACCINATION (ID or IM)

Less than 1 month No booster dose

1 – 5 months 1 booster

More than 6 months – 3 years 2 booster doses (D0, D3)

More than 3 years Full course of active immunization

•

Special conditions:! Pregnancy and infancy are NOT contraindications

! Babies born of rabid mothers should be given vaccine

and RIG as early as possible

! Patients taking chloroquine, anti-epileptics, systemic

steroids, and alcoholic patients should be given standard

IM regimen! All Category II and III immunocompromised patients

should receive standard IM regimen and RIG•

Pre-exposure vaccination (D0!D7!D21/28) is recommended

for individuals at high risk of exposure:

! Rabies diagnostic laboratories

! Veterinarians and veterinary students

! Animal handlers

! Health care workers of rabies patients

! Rabies control personnel

! Children 2 to 10 years old! Field workers

PASSIVE IMMUNIZATION PRODUCTS (RIG)

•

Given to provide immediate neutralizing antibodies to cover

the gap until the appearance of vaccine detectable

antibodies• Total computed RIG should be infiltrated around and into the

wound as much as anatomically feasible even if the lesion has

healed

• Remaining RIG should be administered deep IM at a site

distant from the site of vaccine injection

• Types:

1. Human Rabies Immune Globuline (HRIG) – from plasma of

human donors; Dose = 20 IU/kg

2.

Highly Purified Antibody Antigen Binding Fragments(F(ab’)2) – from equine rabies immune globuline (ERIG);

Dose = 40 IU/kg

3. Equine Rabies Immune Globulin – from horse serum; Dose

= 40 IU/kg

References

1.

Handbook of Medical and Surgical Emergencies, 6th edition2.

Longo, D.L., Fauci, A.C., Kasper, D.L, et al. (2013). Harrison’s

Principles of Internal Medicine, 18th edition. McGraw-Hi

Companies Inc.: New York.

3. San Lazaro Hospital Rotation notes


16/24

30 TETANUS by: toxic JI

Definition:

# Tetanus is an acute, often fatal disease caused by woundcontamination with Clostridium tetani, a motile,

nonencapsulated anaerobic gram-positive rod.

Pathophysiology:

# C. tetani exists in either a vegetative or a spore-forming state.

# The spores are ubiquitous in soil and in animal feces and are

extremely resistant to destruction, surviving on environmental

surfaces for years.# C. tetani is usually introduced into a wound in the spore-forming,

noninvasive state but can germinate into a toxin-producing,

vegetative form if tissue oxygen tension is reduced.

# Factors such as the presence of crushed, devitalized tissue, a

foreign body, or the development of infection favor the growth

of the vegetative, toxin-producing form of C. tetani.

# C. tetani produces two exotoxins.

1st toxin: Tetanolysin o

Which appears to favor the expansion of the bacterial

population, and

2nd toxin: Tetanospasmin

o A powerful neurotoxin that is responsible for all the clinical

manifestations of tetanus. Tetanospasmin is one of the

most potent toxins known

o

Although the infection caused by C. tetani remains

localized to the site of injury, tetanospasmin reaches thenervous system by hematogenous spread of the exotoxin

to peripheral nerves and by retrograde intraneuronal

transport.

o Tetanospasmin acts on the motor end plates of skeletal

muscle, in the spinal cord, brain, and sympathetic nervous

system. This extremely potent exotoxin prevents the release

of the inhibitory neurotransmitters glycine and "-aminobutyric acid (GABA) from presynaptic nerve

terminals, releasing the nervous system from its normal

inhibitory control.

# All of the clinical manifestations of tetanus are

secondary to tetanospasmin, and there is no person-

to-person transmission of the disease

Clinical Features:

#

Tetanus results in generalized muscular rigidity, violent

muscular contractions, and autonomic nervous system

instability.

#

Wounds that become contaminated with toxin-producing C.

tetani are most often puncture wounds, but contaminated

wounds range from deep lacerations to minor abrasions.

# No wound is identified in up to 10% of patients with tetanus.# Tetanus can also develop after surgical procedures, otitis

media, or abortion and can develop in injection drug users

from contaminated heroin and in neonates through infection

of the umbilical stump.

# The incubation period for tetanus ranges from


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C. Muscle Relaxants

# Tetanospasmin prevents neurotransmitter release at inhibitory

interneurons, and therapy of tetanus is aimed at restoring

normal inhibition.# The benzodiazepines are centrally acting inhibitory agents

that have been used extensively for this purpose.

# Give the water-soluble agent, midazolam, for muscle

relaxation. 1st Line!

D. Neuromuscular Blockade

# To control ventilation and muscular spasms as well as to

prevent fractures and rhabdomyolysis, prolongedneuromuscular blockade may be required in the treatment of

tetanus.

# Succinylcholine an be given for emergency airway control,

whereas vecuronium a good option for prolonged blockade

because of minimal cardiovascular side effects.

E. Treatment of Autonomic Dysfunction

# 1st Line- Magnesium sulfate inhibits the release of epinephrineand norepinephrine from the adrenal glands and adrenergic

nerve terminals, eliminating the source of catecholamine

excess in tetanus.

# Labetalol, the combined #- and !-adrenergic blocking agent

has been used successfully in treating the manifestations of

sympathetic hyperactivity of tetanus.

#

Morphine sulfate reduces sympathetic #-adrenergic tone and

central sympathetic efferent discharge and producesperipheral arteriolar and venous dilatation.

# Clonidine, a central #2-receptor agonist, has also been used to

manage tetanus-induced cardiovascular instability.

F. Active Immunization

# Patients who recover from tetanus must receive active

immunization, because the disease does not confer immunity.# Adsorbed tetanus toxoid (0.5 mL) should be administered IM

at the time of presentation and at 6 weeks and 6 months after

injury.

# 2 forms:

o Td (tetanus-dipththeria) - to patients !7 years of age

o DTap (tetanus toxoid, reduced diphtheria toxoid, and

acellular pertussis vaccine) - to children


18/24

32 STROKE by toxic JI

(2 parts siya. ang haba! I tried to make it as short as possible)

# Stroke is a cerebrovascular disorder resulting from impairmentof cerebral blood supply by occlusion (eg, by thrombi or

emboli) or hemorrhage.

# It is characterized by the abrupt onset of focal neurologic

deficits.

# Thus, the definition of stroke is clinical, and laboratory studies

including brain imaging are used to support the diagnosis.

# The clinical manifestation depends on the area of the brain

served by the involved blood vessel.# Stroke is the most common serious neurologic disorder in

adults and occurs most frequently after age 60 years.

# The mortality rate is 40% within the first month, and 50% of

patients who survive will require long-term special care.

Types:

# Stroke is classified as resulting from two major mechanisms:

ischemia and hemorrhage.#

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

categorized by causes as thrombotic, embolic, or

hypoperfusion related.

# Hemorrhagic strokes are subdivided into intracerebral

(accounting for 10% of all strokes) and nontraumatic

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

#

The final common pathway for all these mechanisms is

altered neuronal perfusion.# Neurons are exquisitely sensitive to changes in cerebral blood

flow and die within minutes of complete cessation of

perfusion. This fact underlies the current treatment emphasis

on rapid reperfusion strategies.

# Transient ischemic attack (TIA) – the standard definition of TIA

requires that all neurologic signs and symptoms resolve within

24 hours regardless of whether there is imaging evidence ofnew permanent brain injury; stroke has occurred if the

neurologic signs and symptoms last for >24 hours.

A. Ischemic Stroke

# Ischemic strokes, comprising thrombotic, embolic, and

lacunar occlusions, account for over 80% of all stroke

and result in cerebral ischemia or infarction.

#

A variety of disorders of blood, blood vessels, and hear

can cause occlusive strokes, but the most common by faare atherosclerotic disease (especially of the carotid and

vertebrobasilar arteries) and cardiac abnormalities.

Essentials of Diagnosis

# Secondary to thrombosis or embolism

#

Consider in acute neurologic deficit (focal or global) oaltered level of consciousness

# No historical feature distinguishes ischemic from intracerebrahemorrhagic stroke, although headache, nausea and

vomiting, and altered level of consciousness are more

common in intracerebral hemorrhagic stroke

# Abrupt onset of hemiparesis, monoparesis, or quadriparesis

dysarthria, ataxia, vertigo; monocular or binocular visual loss

visual field deficits, diplopia

Pathophysiology

#

Acute occlusion of an intracranial vessel causes reduction in

blood flow to the brain region it supplies.

#

The magnitude of flow reduction is a function of collatera

blood flow and this depends on individual vascular anatomy

the site of occlusion, and likely systemic blood pressure.

#

A decrease in cerebral blood flow to zero causes death obrain tissue within 4-10 minutes;

# If blood flow is restored prior to a significant amount of cel

death, the patient may experience only transient symptoms

and the clinical syndrome is called a TIA.

# Tissue surrounding the core region of infarction is ischemic bu

reversibly dysfunctional and is referred to as the ischemic

penumbra. The penumbra may be imaged by using

perfusion-diffusion imaging with MRI or CT (see below and

Figs. 370-15 and 370-16). The ischemic penumbra wieventually infarct if no change in flow occurs, and hence

saving the ischemic penumbra is the goal o

revascularization therapies.

Focal cerebral infarction occurs via two distinct pathways: (1) a

necrotic pathway in which cellular cytoskeletal breakdown is rapiddue principally to energy failure of the cell; and (2) an apoptoticpathway in which cells become programmed to die. Ischemia

produces necrosis by starving neurons of glucose and oxygen

which in turn results in failure of mitochondria to produce ATP

Without ATP, membrane ion pumps stop functioning and neurons

depolarize, allowing intracellular calcium to rise. Cellula

depolarization also causes glutamate release from synaptic

terminals; excess extracellular glutamate produces neurotoxicity by

activating postsynaptic glutamate receptors that increaseneuronal calcium influx. Free radicals are produced by membrane

lipid degradation and mitochondrial dysfunction. Free radical

cause catalytic destruction of membranes and likely damage

other vital functions of cells. Lesser degrees of ischemia, as are

seen within the ischemic penumbra, favor apoptotic cellular death


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

brain injury during ischemia, as does hyperglycemia [glucose >11.1

mmol/L (200 mg/dL)], so it is reasonable to suppress fever and

prevent hyperglycemia as much as possible. Induced moderatehypothermia to mitigate stroke is the subject of continuing clinical

research


20/24

48 EPISTAXIS

Definition

• Epistaxis – bleeding from the nose

! Bleeding above the glottis (upper airway source)

! Sensation of pooling of blood in the throat or need to

clear the throat before bleeding

• Nasal blood supply

! Origin 1: External Carotid artery

1. Facial artery! Superior labial artery

! Septum and nasal alae

2.

Internal Maxillary arterya. Sphenopalatine artery

! Septum, middle and inferior turbinates

b. Pharyngeal artery

c. ! Inferior aspect of lateral nasal wall

d. Greater palatine artery

! Anterior aspect of septum

! Origin 2: Internal Carotid artery

1.

Ophthalmic artery! septum and lateral nasal walls2.

Anterior ethmoidal artery

3. Posterior ethmoidal artery

•

Sources of epistaxis:

1. Woodruff area

! Inferior aspect of the lateral nasal wall, posterior to

the inferior turbinate (more posterior

! Sphenopalatine + Pharyngeal arteries

! Common source of severe nontraumatic bleeds

2.

Kiesselbach plexus

! Most common source of nose bleeds

! Anteromedial aspect of the nares

! Anterior ethmoidal + Greater palatine +

Sphenopalatine + Superior labial arteries

Etiology

LOCAL SYSTEMIC

Trauma

Anatomic deformitiese.g. Septal deflections, bony spurs,

fractures*Anything obstructive can lead to

disruption of air flow resulting to turbulent

air flow anterior to the defect causing

draying effect, increasing opportunity for

mucosal disruption

Inflammatory reactionsBacterial sinusitis, allergic rhinitis,

nasal polyposis, Wegner

granulomatosis, Tuberculosis,

Sarcoidosis

Intranasal tumors, vascularmalformations

e.g. Inverted papilloma,

angiofibroma, aneurysm,

encephalocele, hemangioma,

adenocarcinoma

Hypertension

Most common finding in

severe or refractory

epistaxis

Aberrations in clotting abilityMedications – aspirin,

clopidogrel, NSAIDs, warfarin

Inherited bleeding diathesesHemophilia A (Factor VIII)

Hemophilia B (Factor IX)Von Willebrand disease (vWF

is essential to Factor VIII

function)

Vascular/cardiovascular

diseasesCongestive heart failure

Arteriosclerosis

Collagen abnormalities

Clinical manifestations

• Risk factors

! Medications

1. Antiplatelets

2.

Anticoagulants (e.g. Warfarin)

! Renal failure! Hemophilia

! Pre nanc

•

Symptoms

! Easy bruisability

! Bleeding tendencies

• Causes

! Dry conditions created by heated indoor air during cold

season can dehydrate airways and predispose nasal

mucosa to cracking

! Repeated blowing and wiping of nose, blunt trauma,

nose picking can abrade and injure mucosal surface

• Physical examination

! Examine hemodynamically stable patient in sitting

position to allow blood to exit anterior nose and minimizeingestion or aspiration

! Ask patient to clear each nostril of clots then pinch entire

cartilaginous portion of the nose for 15 minutes

continuously

! Insert nasal speculum and examine both sides of the nose

for bleeding and the integrity of the septum

! Observe the posterior oropharynx for 10 to 15 seconds to

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

Treatment

ANTERIOR EPISTAXIS

•

Minimally invasive and technically simple methods are

preferred

•

Gentle opiate or benzodiazepine sedation for vasoconstriction

and local anesthesia! 1% phenylephrine

! 4% cocaine

! 2% lidocaine-epinephrine

• Once bleed visualized! Simple cautery with Silver Nitrate

• Persistent bleeding! Nasal packing with phenylephrine,

cocaine, or lidocaine-epinephrine! Push superiorly until the

nostril is packed•

Or use Nasal tampons

• Give Amoxicillin-clavulanate BID for prophylaxis against

Bacterial sinusitis in patients with nasal pack

• Packing material should be removed in 3 to 5 days

POSTERIOR EPISTAXIS

•

Foley catheter, nasal balloon device inflated to tamponade

bleeding site•

If packing is needed admit for airway observation,

prophylactic antibiotics, ENT consultation

References1. Bailey B. J. Head and Neck Surgery–Otolaryngology. 4th ed.

Philadelphia, PA: Lippincott Williams & Wilkins; 2006. 2.

Current Diagnosis and Treatment: Emergency Medicine, 6 th edition


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50 APPENDICITIS

Definition

Inflammation of the vermiform appendix, ranging from a simplecatarrhal/congestive form to a more complicated transmural

involvement resulting to a perforated appendix

Anatomy

Vermiform Process or Appendix

• A long, narrow, worm-shaped tube

! With a small canal throughout its length that

communicates with the cecum by an orifice below andbehind the ileocecal opening, sometimes guarded by a

semilunar valve

• Function: immunologic – secretes Ig (IgA)

•

Location:

! McBurney’s point : 1/3 of the way up the line joining the

right anterior superior iliac spine to the umbilicus

! Originates from the apex of the cecum

*Trace the taenia coli of the cecum to the base of theapex where they converge to form the longitudinal

muscle coat

! Held in position by the mesenteriole: fold of peritoneum

from the left leaf of the mesentery

! Common positions of the tip of the appendix:

*1 and 2 – most common

1.

Hanging down in the pelvis, against right pelvic wall

2.

Coiled up behind the cecum3.

Projecting upward along lateral side of cecum

4. In front of or behind terminal ileum

•

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

• Nerve supply

! Superior mesenteric plexus:

1. Parasympathetic

2. Sympathetic – afferent (sensory fibers):conduct visceral pain from the appendix, enter

spinal cord at T10

•

Blood supply: Appendicular artery

! Located between the 2 folds of the mesenteriole, close to

the free margin

! Origin: Ileocolic artery, from Superior mesenteric a.

•

Venous drainage: Appendicular vein

! Drains to Ileocolic vein, tributary of Superior mesenteric v.•

Lymph drainage: one or two intermediate nodes in the

mesoappendix, drain to Superior mesenteric LNs

Histology

1. Serous

•

Complete except along the line of attachment of the

mesenteriole2.

Muscular

• Longitudinal muscle fibers

! Does not form 3 bands unlike rest of large intestine

! Complete except at one or two points that allow

contiguity of peritoneal and submucous coats

• Circular muscle fibers – thicker layer

3. Submucous

• Contains large number of masses of lymphoid tissue

which may cause mucous membrane to bulge into thelumen and decrease its size

4. Mucous

•

Columnar epithelium

• Fewer intestinal glands compared to rest of large intestine

Etiology

• Dominant etiologic factor – obstruction of the lumen

•

Most common cause of obstruction – Fecaliths: accumulation

and inspissation of fecal matter around vegetable fibers

•

Other causes of obstruction:

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

! Inspissated barium from previous X-ray studies

! Tumors

! Ve etable and fruit seeds

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

• Other etiologic factors:

! Infection with Yersinia: high complement fixation

Pathogenesis

Stages of Appendicitis

1.

UNCOMPLICATED • Congestive or Catarrhal – due to mucosal and

submucosal inflammation only

• Suppurative – the whole appendix becomes swollen,

turgid, and loses its healthy sheen and is coated with a

fibrinous exudate

2.

COMPLICATED

• Gangrenous – due to unrelieved obstruction, the capillary

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

• Perforative – if gangrenous appendicitis is not treated,

then perforation may ensue and take one of the following

two events:

! Outporuring of inflammatory cells and mediators

from parietal peritoneum and serosa of adjacent

visceral structures may confine the perforation and

eventually lead to a walling off effect leading to aformation of periappendicial abscess

! Failure of the above mechani

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