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Transcript of Batch 1b.pdf
![Page 1: Batch 1b.pdf](https://reader034.fdocuments.us/reader034/viewer/2022052217/577cc3691a28aba71195f868/html5/thumbnails/1.jpg)
Signs & Symptoms
Swelling & tenderness inthe abdomen
Fever & Chills
Loss of Appetite
Nausea & Vomiting
Increased breathing &Heart Rates
Shallow Breaths
Low BP
Limited Urine Production
Inability to pass gas orfeces
Exam :
The usual sounds made bythe active intestine andheard during examinationwith a stethoscope will beabsent, because theintestine usually stopsfunctioning.
The abdom may be rigidand boardlike
Accumulations of fluid willbe notable in primary dueto ascites.
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Evaluation
Lab :
Blood Test
Samples of fluid from
the abdomen
CT Scan
Chest X-rays
Peritoneal lavage.
th/
Hospitalization is
common.
Surgery is often
necessary to remove thesource of infection.
Antibiotics are
prescribed to control theinfection & intravenoustherapy (IV) is used torestore hydration.
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Stomach/duodenum – Perforation
Presentation :
abdominal pain
Pain on palpation
Release pain
rigidity
peritonism, shock
Air under diaphragm onX-ray
Treatment
resuscitateantibiotics,
repair
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Mekanisme Sekresi Asam lambung
optimized by optima
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Blunt Abdominal Trauma
The most commonly injured organs
Spleen
Liver
Retroperitoneum
small bowel
kidneys
Bladder
Colorectum
Diaphragm
pancreas
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32. Shock
Cardiogenic shock - a major component of the the
mortality associated with cardiovascular disease (the
#1 cause of U.S. deaths)
Hypovolemic shock - the major contributor to early
mortality from trauma (the #1 cause of death in those
< 45 years of age)
Septic shock - the most common cause of death in
American ICUs (the 13th leading cause of death overall
in US)
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Shock: Definitions
Kumar and Parrillo (1995) - ―The state in which
profound and widespread reduction of effective tissue
perfusion leads first to reversible, and then if
prolonged, to irreversible cellular injury.‖
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Shock: Classification
Hypovolemic shock - due to decreased circulating blood volume in
relation to the total vascular capacity and characterized by a reductionof diastolic filling pressures
Cardiogenic shock - due to cardiac pump failure related to loss of
myocardial contractility/functional myocardium or structural/ mechanicalfailure of the cardiac anatomy an characterized by elevations ofdiastolic filling pressures and volumes
Extra-cardiac obstructive shock - due to obstruction to flow in the
cardiovascular circuit and characterized by either impairment of diastolicfilling or excessive afterload
Distributive shock - caused by loss of vasomotor control resulting in
arteriolar/venular dilatation and characterized (after fluid resuscitation)by increased cardiac output and decreased SVR
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Hypovolemic
Hemorrhagic
Trauma
Gastrointestinal
Retroperitoneal
Fluid depletion
(nonhemorrhagic)
External fluid loss
Dehydration
Vomiting
Diarrhea
Polyuria
Interstitial fluid redistribution
Thermal injury
Trauma
Anaphylaxis
Increased vascular
capacitance (venodilatation)
Sepsis
Anaphylaxis
Toxins/drugs
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CARDIOGENIC
Myopathic
Blunt Cardiac Injury (trauma)
Myocarditis
Cardiomyopathy
Post-ischemic myocardial
stunning
Septic myocardial depression
Pharmacologic : Calcium
channel blockers
Mechanical
Valvular failure (stenotic or
regurgitant)
Hypertropic cardiomyopathy
Ventricular septal defect
Arrhythmic
Bradycardia
Tachycardia
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EXTRACARDIAC OBSTRUCTIVE
Impaired diastolic filling
(decreased ventricular preload)
Direct venous obstruction (vena
cava)
intrathoracic obstructive
tumors
Increased intrathoracic pressure
Tension pneumothorax
Mechanical ventilation (with
excessive pressure or volumedepletion)
Asthma
Decreased cardiac compliance
Constrictive pericarditis
Cardiac tamponade
Impaired systolic contraction
(increased ventricular afterload)
Right ventricle
Pulmonary embolus (massive)
Acute pulmonary
hypertension
Left ventricle
embolus
Aortic dissection
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DISTRIBUTIVE
Septic (bacterial, fungal, viral, rickettsial)
Toxic shock syndrome
Anaphylactic, anaphylactoid
Neurogenic (spinal shock)
Endocrinologic
Adrenal crisis
Thyroid storm
Toxic (e.g., nitroprusside, bretylium)
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• Cutaneous vasoconstriction vs. vasodilation.
• Mental Changes: anxiousness, agitation, indifference,
CLINICAL MARKERS OF SHOCK
l
kj
• Brachial systolic blood pressure: <110mmHg
• Sinus tachycardia: >90 beats/min
• Respiratory rate: <7 or >29 breaths/min
• Urine Output: <0.5cc/kg/hr
• Metabolic acidemia: [HCO3]<31mEq/L or base
deficit>3mEq/L
• Hypoxemia: 0-50yr: <90mmHg; 51-70yr: <80mmHg;>71yo<70mmHg; K
lethargy, obtundation
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Etiologyofshock example CVP CO SVR VO2sat
preload hypovolemic low low high low
contractility cardiogenic high low high low
afterload distributive
Etiology & Hemodynamic Changes in Shock
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ETIOLOGYOF
SHOCK
EXAMPLE CVP CO SVR VO2SAT
AFTERLOAD DISTRIBUTIVE
HyperdynamicSeptic Low/High High Low High
HypodynamicSeptic Low/High Low High Low/High
Neurogenic Low Low Low Low
Anaphylactic Low Low Low Low
Etiology & Hemodynamic Changes in Shock
(Afterload)
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HYPOVOLEMIC SHOCK• Decreased preload->small ventricular end-diastolic
volumes -> inadequate cardiac generation of pressure andflow
• Causes:
• bleeding: trauma, GI bleeding, ruptured aneurysms,
hemorrhagic pancreatitis
• protracted vomiting or diarrhea
• adrenal insufficiency; diabetes insipidus
• Dehydration
• third spacing: intestinal obstruction, pancreatitis,cirrhosis
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Hypovolemic Shock
Signs & Symptoms: Hypotension, Tachycardia, MSchange, Oliguria, Deminished Pulses.
Markers: monitor UOP,CVP, BP, HR, Hct, MS, CO, lacticacid and PCWP
Treatment: ABCs, IVF (crystalloid), Trasfusion Stemongoing Blood Loss
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SEPTIC/INFLAMMATORY SHOCK
Mechanism: release of inflammatory mediators leading to
1. Disruption of the microvascular endothelium
2. Cutaneous arteriolar dilation and sequestration of blood incutaneous venules and small veins
Causes:
1. Anaphylaxis, drug, toxin reactions
2. Trauma: crush injuries, major fractures, major burns.
3. infection/sepsis: G(-/+ ) speticemia, pneumonia, peritonitis,
meningitis, cholangitis, pyelonephritis, necrotic tissue,pancreatitis, wet gangrene, toxic shock syndrome, etc.
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Septic/Inflammatory Shock
Signs: Early– warm w/ vasodilation, often adequate urine
output, febrile, tachypneic.
Late-- vasoconstriction, hypotension, oliguria,
altered mental status.
Monitor/findings: Early—hyperglycemia, respiratory
alkylosis, hemoconcentration,WBC typically normal or low.
Late – Leukocytosis, lactic acidosis
Very Late– Disseminated Intravascular
Coagulation & Multi-OrganSystem Failure.
Tx : ABCs, IVF, Blood cx, ABX, Drainage (ie abscess)
pressors.
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CARDIOGENIC SHOCK
Mechanism: Intrinsic abnormality of heart -> inability todeliver blood into the vasculature with adequate power
Causes:
1. Cardiomyopathies: myocardial ischemia, myocardial infarction,cardiomyopathy, myocardiditis, myocardial contusion
2. Mechanical: cardiac valvular insufficiency, papillary muscle rupture,septal defects, aortic stenosis
3. Arrythmias: bradyarrythmias (heart block), tachyarrythmias (atrialfibrillation, atrial flutter, ventricular fibrillation)
4. Obstructive disorders: PE, tension peneumothorax, pericardialtamponade, constrictive pericaditis, severe pulmonary hypertension
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Cardiogenic Shock
Characterized by high preload (CVP) with low CO
Signs/SXS: Dyspnea, rales, loud P2 gallop, low BP, oliguria
Monitor/findings: CXR pulm venous congestion, elevated CVP,
Low CO.
Tx: CHF– diuretics & vasodilators +/- pressors.
LV failure – pressors, decrease afterload,
intraaortic ballon pump &
ventricular assist device.
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NEUROGENIC SHOCK
Causes:
1.Spinal cord injury
2.Regional anesthesia
3.Drugs
4.Neurological disorders
Mechanism: Loss of autonomic
innervation of the cardiovascular system(arterioles, venules, small veins, includingthe heart)
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Neurogenic Shock
Characterized by loss of vascular tone & reflexes.
Signs: Hypotension, Bradycardia, Accompanying
Neurological deficits.
Monitor/findings: hemodynamic instability, test
bulbo-carvernous reflex
Tx: IVF, vasoactive medications if refractory
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33. FOREHAND FRACTURE
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Montegia Fracture Dislocation
It is a fracture of the proximal
1/3rd of the Ulna with
dislocation of head of radius
anteriorly. Posteriorly or
laterally
Head of Radius dislocates
same direction as fracture
It requires ORIF or it will
redisplace
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Montegia : Lateral displacement
optimized by optima
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Galliazi Fracture
It is a fracture of distal
Radius and dislocation ofinferior Radio- Ulnar joint
Like Montegia fracture if
treated conservatively itwill redisplace
This fracture appeared in
acceptable position afterreduction and POP
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Greenstick Fractures
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Colles‘ Fracture
Most common fracture in Osteoporoticbones
Extra-Articular : 1 inch of distal Radius
Results from a fall on dorsi flexed wrist
Typical deformity : Dinner Fork
Deformity is : Impaction, dorsal displacement
and angulation, radial displacement andangulation and avulsion of ulnar styloidprocess
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Colles‘ Fracture
optimized by optima
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# distal 1‘‘ Impaction ,Dorsal displacement
and dorsal tilt
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Colles‘ Fracture
optimized by optima
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Smith Fracture
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Smith Fracture
Almost the opposite of Colles‘ fracture
Much less common compared to colles‘
Results from a fall on palmer flexed wrist
Typical deformity : Garden Spade
Management is conservative : MUA and Above
Elbow POP
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34. LOW BACK PAIN
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Herniated Nucleus Pulposus
The progressive
degeneration of a disc, or
traumatic event, can lead
to a failure of the annulus
to adequately contain the
nucleus pulposus
This is known as herniated
nucleus pulposus (HNP) or
a herniated disc
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Herniated Nucleus Pulposus
Symptoms
Back pain
Leg pain
Dysthesias
Anesthesias
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Herniated Nucleus Pulposus
Varying degrees
Disc bulge
Mild symptoms
Usually go away with
nonoperative treatment
Rarely an indication
for surgery
Extrusion (herniation)
Moderate/severe symptoms
Nonoperative treatment
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Herniated Nucleus Pulposus
Diagnosis
Magnetic resonance imaging(MRI)/patient exam
Nonoperative Care
Initial bed rest
Nonsteroidal anti-
inflammatory (NSAID)medication
Physical therapy
Exercise/walking
Steroid injections
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Herniated Nucleus Pulposus
Surgical care
Failure of nonoperative
treatment
of 6 weeks in Minimumduration
Can be months
Discectomy
Removal of the
herniatedportion of the disc
Usually through a small
incision
High success rate
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Herniated Nucleus Pulposus
Cauda Equina Syndrome
Caused by a central disc
herniation
Symptoms include bilateral
leg pain, loss of perianal
sensation, paralysis of the
bladder, and weakness of
the anal sphincter
Surgical intervention in
these cases is urgent
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Spondylolisthesis
Gradation of
spondylolisthesis
Meyerding‘s Scale
Grade 1 = up to 25%
Grade 2 = up to 50%
Grade 3 = up to 75%
Grade 4 = up to 100%
Grade 5 >100%
(complete dislocation,
spondyloloptosis)
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Spondylolisthesis
Symptoms
Low back pain
With or without buttock or
thigh pain
Pain aggravated by standing
or walking
Pain relieved by lying down
Concomitant spinal stenosis,
with or without leg pain, maybe present
Other possible symptoms
Tired legs, dysthesias,
anesthesias
Partial pain relief by leaning
forward or sitting
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Spondylolisthesis
Diagnosis
Plain radiographs
CT, in some cases with
leg symptoms
Nonoperative Care
Rest
NSAID medication
Physical therapy
Steroid injections
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Spondylolisthesis
Surgical care
Failure of nonoperative
treatment
Decompression and fusion
Instrumented
Posterior approach
With interbody fusion
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Spondylolysis
Spondylolysis
Also known as pars defect
Also known as pars fracture
With or without
spondylolisthesis
A fracture or defect in the
vertebra, usually in the
posterior elements—most
frequently in the pars
interarticularis
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Spondylolysis
Symptoms
Low back pain/stiffness
Forward bending
increases pain
Symptoms get worse
with activity
May include a stenotic
component resulting in
leg symptoms
Seen most often in athletes
Gymnasts at risk
Caused by repeated strain
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Spondylolysis
Diagnosis
Plain oblique radiographs
CT, in some cases
Nonoperative care
Limit athletic activities
Physical therapy
Most fractures heal without
other medical intervention
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Spondylolysis
Surgical care
Failure of nonoperative treatment
Posterior fusion
Instrumented
May require decompression
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Ankylosing spondilitis
optimized by optima
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35. ABDOMINAL INJURIES
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Causes
injuries to the
abdomen, pelvis
and genitalia are
generally caused by
accidents involving
high kinetic energy
and acceleration or
deceleration forces
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Open vs. Closed Injuries
Abdominal injuries can beeither open or closed
Open injuries are caused bysharp or high velocityobjects that create anopening between theperitoneal cavity and theoutside of the body
Closed injuries are causedby compression traumaassociated withdeceleration forces andinclude:
contusions
ruptures
lacerations
shear injuries
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Hollow and Solid Organs
The type of injury will depend on whether the organ injured issolid or hollow.
hollow organs include:
stomach
intestines
gallbladder
bladder
solid organsinclude:
liver
spleen
kidneys
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when hollow organsrupture, their highlyirritating andinfectious contentsspill into theperitoneal cavity,producing a painfulinflammatory reactioncalled peritonitis
damage to solid organssuch as the liver can causesevere internal bleeding
blood in the peritonealcavity causes peritonitis
when patients injure solidorgans, the symptoms ofshock may overshadowthose from peritonitis
Abdominal Injuries
Hollow Organ Injuries Solid Organ Injuries
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Abdominal Injuries
Abdominal injuries canbe obvious, such as anopen wound, or subtle,such as a blow to theflank that initiallycauses little pain, butdamages the liver orspleen
Suspect abdominalinternal injury in anypatient who has apenetrating abdominalwound or has sufferedcompression trauma tothe abdomen
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Liver
Largest organ in abdominalcavity
Right upper quadrant
Injured from trauma to: Eighth through twelfthribs on right side ofbody
Upper central part ofabdomen
Suspect liver injury when:
Steering wheel injury Lap belt injury Epigastric trauma
After injury, blood and bileleak into peritoneal cavity Shock
Peritoneal irritationManagement:
Resuscitation Laparotomy and repairor resection.
Avulsion of pedicle isfatal
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Spleen
Upper left quadrantRich blood supply
Slightly protected by organssurrounding it and by lower ribcage Most commonly injured organ
from blunt trauma Associated intraabdominal
injuries commonSuspect splenic injury in:
Motor vehicle crashes Falls or sports injuries
involving was an impact to thelower left chest, flank, orupper left abdomen
Kehr’s sign
Left upper quadrant painradiates to left shoulder
Common complaint withsplenic injury
Management :
Resuscitation.
Laparotomy (repair, partialexcision or splenectomy)
Observation in hospital forpatients with sub-capsularhaematoma
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Stomach/duodenum
Not commonly injured by blunt trauma
Protected location in abdomen
Penetrating trauma may cause gastric transection or
laceration
Signs of peritonitis from leakage of gastric contents
Diagnosis confirmed during surgery
Unless nasogastric drainage returns blood
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Stomach/duodenum
Presentation :
abdominal pain
rigidity
peritonism, shock
Air under diaphragm onX-ray
Treatment Antibiotics
resuscitate
repair
Presentation :
Haematemesis +/-
Melaena
Severity
Increased PR>90
Fall BP<100
Treatment :
transfusion
inject DU
Perforation Bleeding
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36. ILEUS
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Introduction and Definitions
Accounts for 5% of all acute surgical admissions
Patients are often extremely ill requiring prompt
assessment, resuscitation and intensive monitoring
Obstructive ileus
A mechanical blockage arising from a structural abnormality
that presents a physical barrier to the progression of gut
contents.Paralytic Ileus
is a paralytic or functional variety of obstruction
Obstruction is: Partial or complete
Simple or strangulated
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Pathophysiology I
8L of isotonic fluid received by the small intestines (saliva,stomach, duodenum, pancreas and hepatobiliary )7L absorbed
2L enter the large intestine and 200 ml excreted in the faeces
Air in the bowel results from swallowed air ( O2& N2) and bacterialfermentation in the colon ( H2, Methane & CO2),
600 ml of flatus is releasedEnteric bacteria consist of coliforms, anaerobes and strep.faecalis.
Normal intestinal mucosa has a significant immune role
Distension results from gas and/ or fluid and can exert hydrostaticpressure.In case of BO Bacterial overgrowth can be rapid
If mucosal barrier is breached it may result in translocation of bacteria andtoxins resultingin bactaeremia,septaecemia and toxaemia.
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Pathophysiology II
Obstruction results in:
1.
2.
3.
4.
5.
6.
7.
8.
Initial overcoming of the obstructionby increased paristalsisIncreased intraluminal pressure by fluid and gasVomitingsequestrationof fluid into the lumen from the surroundingcirculationLymphatic and venous congestion resultingin oedematous tissuesFactors 3,4,5 result in hypovolaemia and electrolyte imbalanceFurther: localised anoxia,mucosal depletion necrosisand perforationand peritonitis.Bacterial over growth with translocation of bacteria and it’s toxinscausingbacteraemia and septicaemia.
Decompresswith NGTReplace lost fluid
Correct electrolyteabnormalities
Recognisestrangulation andperforation
Systemic antibiotics.
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Colonic
• Preexisting change in
bowel habit
•Colicky in the lower
abdomin
•Vomiting is late
•Distension prominent
•Cecum ? distended
Distal small bowel
•Pain: central and colicky
•Vomitus is feculunt
•Distension is severe
•Visible peristalsis
•May continue to pass
flatus and feacus before
absolute constipation
High
•Pain is rapid
•Vomiting copious and
contains bile jejunal content
•Abdominal distension is
limited or localized
•Rapid dehydration
1. History
The Universal Features
Colicky abdominal pain, vomiting, constipation (absolute), abdominal
distension.
Complete HX ( PMH, PSH, ROS, Medication, FH, SH)
Persistent pain may be a sign of strangulation
Relative and absolute constipation
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Luminal Mural Extraluminal
F.Body
Bezoars
Gallstone
FoodParticles
A.lumbricoides
Neoplasms
lipoma
polyps
leiyomayoma
hematoma
lymphoma
carcinoid
carinoma
secondaryTumors
Crohns
TB
Stricture
Intussusception
Congenital
Postoperative
adhesions
Congenital
adhesions
Hernia
Volvulus
Causes- Small Bowel
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2. Examination
Others
Systemic examination
If deemed necessary.
•CNS
•Vascular
•Gynaecological
•muscuoloskeltal
Abdominal
•Abdominal distension
and it‘s pattern
•Hernial orifices
•Visible peristalsis
•Cecal distension
•Tenderness, guarding
and rebound
•Organomegaly
•Bowel sounds
–High pitched
–Absent
•Rectal examination
General
•Vital signs:
P, BP, RR, T, Sat
•dehydration
•Anaemia, jaundice, LN
•Assessment of vomitus if
possible
•Full lung and heart
examination
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Initial Management in the ER
Resuscitate:
Air way (O2 60-100%)
Insert 2 lines if necessary
IVF : Crytloids at least 120 ml/h. (determined by estimated fluid loss and
cardiac function).Add K+ at 1mmmol/kg
Draw blood for lab investigations
Inform a senior member in the team.
NPO.
Decompress with Naso-gastric tube and secure in position
Insert a urinary catheter (hourly urinary measurements) and start a fluid
input / output chart
Intravenous antibiotics (no clear evidence)
If concerns exist about fluid overloading a central line should be inserted
Follow-up lab results and correction of electrolyte imbalance
The patient should be nursed in intermediate care
Rectal tubes should only be used in Sigmoid volvulus.
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Indications for Surgery
Immediate intervention:
Evidence of strangulation (hernia….etc)
Signs of peritonitis resulting from perforation or
ischemia
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Paralytic Ileus
Associated with the following conditions:
Postoperative and bowel resection
Intraperitoneal infection or inflammation
Ischemia
Extra-abdominal: Chest infection, Myocardia infarction
Endocrine: hypothyroidism, diabetes
Spinal and pelvic fractures
Retro-peritoneal haematoma
Metabolic abnormalities:
Hypokalaemia
Hyponatremia
Uraemia
Hypomagnesemia
Bed ridden
Drug induced: morphine, tricyclic antidepressants
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Clinical Findings
Clinical features
Is there an under lying cause?
Is the abdomen distended but tenderness is not marked.
Is the bowel sounds diffusely hypoactive.
Radiological features:
Is the bowel diffusely distended
Is there gas in the rectum
Are further investigasions (CT or Gastrografin studies) helpful
in showing an obstruction.
Does the patient improve on conservative measures
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37. BURN INJURY
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Burn Injuries
Potential complications
Fluid and Electrolyte loss Hypovolemia
Hypothermia, Infection, Acidosis
catecholamine release, vasoconstriction
Renal or hepatic failure
Formation of eschar
Complications of circumferential burn
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Burn Injuries
An important step inmanagement is todetermine depth andextent of damage todetermine where and howthe patient should betreatedDepth Classification Superficial Partial thickness Full thickness
Thermal burn Skin injury Inhalation injury
Chemical burn Skin injury Inhalation injuryMucous membraneinjury
Electrical burn Lightning
Radiation burn
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Burn Classifications
1st degree (Superficial burn)
Involves the epidermis
Characterized by reddening
Tenderness and Pain
Increased warmth
Edema may occur, but no
blistering
Burn blanches under pressure
Example - sunburn
Usually heal in ~ 7 days
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Burn Classifications
2nd degree
Damage extends through the
epidermis and involves the dermis.
Not enough to interfere with
regeneration of the epithelium
Moist, shiny appearance
Salmon pink to red color
Painful
Does not have to blister to be 2nd
degree
Usually heal in ~7-21 days
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Burn Classifications
3rd degree
Both epidermis and dermis are
destroyed with burning into SC fat
Thick, dry appearance
Pearly gray or charred black color
Painless - nerve endings are destroyed
Pain is due to intermixing of 2nd
degree
May be minor bleeding
Cannot heal and require grafting
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Burn Injuries
Often it is not possible to predict the exact depth of
a burn in the acute phase. Some 2nd degree burns
will convert to 3rd when infection sets in. When in
doubt call it 3rd degree.
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Body Surface Area Estimation
Rule of Nines
Adult
Palm Rule
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Body Surface Area Estimation
Rule of Nines
Peds
For each yr over 1 yoa,
subtract 1% from head
and add equally to legs
Palm Rule
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38. ARTERIAL DISEASE
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Arterial Disease
Raynaud phenomenon is a
vasospastic disease of the digital
arteries; occurs in susceptible
people when exposed to cool
temperatures or during emotional
stress.
Symptoms:
numbness,
paresthesias, or
Pain
Raynaud's syndrome is used to
encompass both the primary &secondary conditions causing
Raynaud phenomenon.
Vasospasm of digital arteriesobliterates the lumen
Inhibited blood flow triphasic colorresponse
fingers blanch to a distinct white as bloodflow is interrupted
cyanosis, related to local accumulation ofdesaturated hemoglobin
ruddy color as blood flow resumes
Lilly LS. Pathophysiology of heart disease. 5th ed. Lipincott William & Wilkins; 2011.
Brunicardi FC. Schwartz principles of surgery. 8th ed. McGraw-Hill; 2004.
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Arterial Disease
Raynaud disease:
Predominantly woman ages 20-40
Mechanism:
sympathetic discharge in
response to cold,
vascular sensitivity to adrenergic
stimuli, or
Raynaud phenomenon:
may appear as a component of otherconditions.
Causes: connective tissue diseases
(scleroderma & SLE) arterial occlusive disorders. carpal tunnel syndrome, thermal or vibration injury.
In patients with connective tissuediseases/arterial occlusive disease: thedigital vascular lumen is largelyobliterated by sclerosis or
Treatment:
sympathetically mediatedvasoconstriction.
footwear.• Preventing vasospasm with CCB or alpha
blocker.Lilly LS. Pathophysiology of heart disease. 5th ed. Lipincott William & Wilkins; 2011.
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39. Urine Incontinence
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40. Urethral Trauma
Anterior Urethral Trauma
Position : Distal fromurogenital diagphram
Etiology :
Straddle Injury
Instrumentation
Clinical Signs :
Blood from urethral meatus
Hematom, perineal pain
Urinary retenstion
Radiology : urethrogram
Therapy :
Sistostomyimmediate repair
Tanagho EA, et al. Smith‘s general urology. 17th ed. McGraw-Hill; 2008.
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Tanagho EA, et al. Smith‘s general urology. 17th ed. McGraw-Hill; 2008.
Urethral Trauma
Posterior Urethral Trauma
Etiology Pelvic bone fracture
Clinical Symptoms Blood from meatus Urinary retention Pain, hematom on pubic region
Radiology Pelvic Photo Urethrogram
Therapy Sistostomy Repair 3-4 days later.
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41. Pericardial Disease
Etiology of cardiac tamponade:
neoplastic, postviral, & uremicpericarditis.
Acute hemorrhage into
pericardium:
blunt/penetrating chest
trauma,
rupture of the left
ventricular free wallfollowing MI,
dissecting aortic aneurysm
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Pulsus Paradoxusdecreased of SBP ≥10 mmHg during inspiration
Thorax expansion duringinspiration
Intrathoracic pressure becomemore negative
Facilitates venous return &right ventricle filling
Increase in RV sizediminishes LV filling
In cardiac tamponade, the normal
situation (left diagram) is
exaggerated because both ventricles
share a reduced, fixed volume as a
result of external compression by the
tense pericardial fluid.
Pulsus paradoxus may also be
manifested by other conditions in
which inspiration is exaggerated,
including severe asthma & COPD.
LV stroke volume & systolicblood pressure decline slightly
McPhee SJ, et al. Pathophysiology of disease. 5th ed. McGraw-Hill; 2006.
Silbernagl S. Color atlas of pathophysiology. 1st ed. Thieme; 2000.
Lilly LS. Pathophysiology of heart disease. 5th ed. Lipincott William & Wilkins; 2011.
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Management:
ABC‘s with c-spine control
as indicated
High Flow oxygen
Cardiac Monitor
Large Bore IV access
Rapid Transport
What patient needs is
pericardiocentesis
Cardiac Tamponade
Pericardiosentesis
Using aseptic technique, Insert atleast 3‖ needle at the angle of theXiphoid Cartilage at the 7th rib
Advance needle at 45 degreetowards the clavicle whileaspirating syringe till blood returnis seen
Continue to Aspirate till syringe isfull then discard blood andattempt again till signs of no moreblood
Closely monitor patient due tosmall about of blood aspiratedcan cause a rapid change in bloodpressure
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42. COMPARTMENT SYNDROME
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Compartment Syndrome
A condition in whichincreased pressure withina limited spacecompromises thecirculation and functionof the tissues within thatspace.
Elevated tissue pressurewithin a closed fascialspace
Reduces tissue perfusion- ischemia
Results in cell death -
necrosis
True Orthopaedic Emergency
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Compartment Syndrome
Etiology
Compartment Size tight dressing; Bandage/Cast
localised external pressure; lying on limb
Closure of fascial defects
Compartment Content Bleeding; Fx, vas inj, bleeding disorders
Capillary Permeability;
Ischemia / Trauma / Burns / Exercise / Snake Bite /Drug Injection / IVF
optimized by optima
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optimized by optima
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optimized by optima
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Compartment SyndromeEtiology
Fractures-closed and
open
Blunt trauma
Temp vascular
occlusion
Cast/dressing
Closure of fascial
defects
Burns/electrical
Exertional states
IV/A-lines
Intraosseous IV(infant)
Snake bite
Arterial injury
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Compartment SyndromeDiagnosis
Pain out of proportion
Palpably tense compartment
Pain with passive stretch
Paresthesia/hypoesthesia
Paralysis
Pulselessness/pallor
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Clinical Evaluation
―Pain and the aggravation of pain by passive
stretching of the muscles in the compartment in
question are the most sensitive (and generally the
only) clinical finding before the onset of ischemic
dysfunction in the nerves and muscles.‖
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Clinical Evaluation
Pain – most important. Especially pain out of
proportion to the injury (child becoming more and
more restless /needing more analgesia)
Most reliable signs are pain on passive stretching
and pain on palpation of the involved compartment
Other features like pallor, pulselessness, paralysis,
paraesthesia etc. appear very late and we should
not wait for these things.
Willis &Rorabeck OCNA 1990
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Compartment SyndromePressure Measurements
Infusion
manometer
saline
3-way stopcock(Whitesides, CORR
1975)
Catheter
wick
slit wick
Arterial line
16 - 18 ga.Needle
(5-19 mm Hg higher)
transducer
monitor
Stryker device
Side port needle
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Compartment SyndromeEmergent Treatment
Remove cast or dressing
Place at level of heart
(DO NOT ELEVATE to optimize perfusion)
Alert OR and Anesthesia
Bedside procedure
Medical treatment
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Surgical Treatment
optimized by optima
Fasciotomy
Casts and tightbandagesremove or
loosen anyconstrictingbandages
All compartments !!!
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PEMBAHASAN ANAK
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43. Ikterus Neonatorum
Bayi perempuan (neonatus), kuning
Lahir cukup bulan, APGAR 5/8
Ibu B Rh-, ayah O Rh+
Hb 15, bilirubin total 8, golongan darah O
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Metabolisme bilirubin
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Bilirubin
Tidak terkonjugasi:
Bilirubin indirek
Tidak larut dalam air
Berikatan dengan albumin
untuk transport
Komponen bebas larut
dalam lemak
Komponen bebas bersifat
toksik untuk otak
Terkonjugasi:
Bilirubin direk
Larut dalam air
Tidak larut dalam lemak
Tidak toksik untuk otak
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Ikterus neonatorum
Secara umum penyebabnya:
Meningkatnya produksi bilirubin akibat hemolisis
Kurangnya albumin sebagai alat transport
Penurunan uptake oleh hati
Penurunan konjugasi bilirubin oleh hati
Penurunan ekskresi bilirubin
Peningkatan sirkulasi enterohepatik
Setiap penyakit yang menyebabkan hemolisis yang
berlebihan atau gangguan pada metabolisme/ekskresibilirubin biasanya akan menyebabkan ikterus
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Ikterus fisiologis vs non fisiologis
Ikterus fisiologis:
Awitan terjadi setelah 24 jam
Memuncak dalam 3-5 hari, menurun dalam 7 hari (pada NCB)
Ikterus fisiologis berlebihan ketika bilirubin serum puncak adalah 7-15 mg/dl pada NCB
Ikterus non fisiologis:
Awitan terjadi sebelum usia 24 jam
Tingkat kenaikan > 0,5 mg/dl/jam
Tingkat cutoff > 15 mg/dl pada NCB
Ikterus bertahan > 8 hari pada NCB, > 14 hari pada NKB
Tanda penyakit lain
Gangguan obstruktif menyebabkan hiperbilirubinemia direk.Ditandai bilirubin direk > 2 mg/dl. Penyabab: kolestasis, atresiabilier, kista duktus koledokus.
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Kemungkinan besar: inkompatibilitas ABO, Rh, penyakit hemolitik, atausferositosis. Penyebab lebih jarang: infeksi kongenital, defisiensi G6PD
Ikterus yang berkembang cepat setelah usia 48 jam
Kemungkinan besar: infeksi, defisiensi G6PD. Penyebab lebih jarang:inkompatibilitas ABO, Rh, sferositosis.
20
18
16
14
12
10
8
6
4
2
0
hari 1 hari 2 hari 3 hari 4 hari 5 hari 6 hari 7
Ikterus yang berkembang cepat pada hari ke-1
fisiologis
non- fisiologis
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Daerah tubuh
Muka
Dada/punggung
Perut dan paha
Tangan dan kaki
Kadar bilirubin (mg/dl)
4 -8
5 -12
8 -16
11-18
Telapal tangan/kaki >15
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Penyakit Keterangan
InkompatibilitasABO Adanyaaglutininibuyangbersirkulasididarahanak
terhadapaglutinogenABOanak.
InkompatibilitasRh Adanyaantibodiibuyangbersirkulasididarahanak
terhadapantigenRhanak.Jarangpadaanakpertama.
Hematomadarah
ekstravaskuler
Akibatprosespersalinan.
DefisiensiG6PD PenyakitterkaitkromosomX.EnzimG6PDberfungsiuntuk
melindungieritrositdarikerusakanoksidatif.
Sferositosisherediter Terdapatdefekproteinmembranyangmenyebabkan
instabilitaseksoskeletoneritrosit
Polisitemia Peningkatanpembentukaneritrosityangmenyebabkan
peningkatandestruksieritrosit
Penyebab hemolisis
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44. Perdarahan pada neonatus
Bayi usia 2 hari
BAB berdarah, muntah darah, petekie
Persalinan ditolong dukun
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Stadium Characteristic
EarlyHDN Occurswithin2daysandnotmorethan5daysoflife.Baby
bornofmotherwhohasbeenoncertaindrugs:anticonvulsant,
antituberculousdrug,antibiotics,VKantagonistanticoagulant.
ClassicHDN Occursduring2to7dayoflifewhentheprothrombincomplex
islow.ItwasfoundinbabieswhodonotreceivedVKPor
VKsupplemented.
VitKdeficiency Occurswithin2daysandnotmorethan5daysoflife.Definite
etiologyinducingVKPisfoundinassociationwithbleeding:
malabsorptionofVKiegutresection,biliaryatresia,severe
liverdisease-inducedintrahepaticbiliaryobstruction.
LateHDN/APCD Acquiredbleedingdisorderinthe2weekto6monthageinfant
causedbyreducedvitaminKdependentclottingfactor(II,VII,
IX,X)withahighincidenceofintracranialhemorrhageand
respondstoVK.
Hemorrhagic disease of newborn (HDN)
Acquired prothrombrin complex deficiency (APCD)
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45. Anemia
Anak perempuan, usia 2 tahun, pucat, rewel, nafsu
makan berkurang
Gizi kurang, anemia, atrofi papila lidah, tidak ada
hepatosplenomegali & limfadenopati
Hb 6,2; leukosit 8.000; Ht 19,5%; tro 350.000;
MCV 62; MCH 21; MCHC 28
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Parameter Kadarnormal Satuan
Hb 6bln-2thn:10,5-13,5
2-6thn:11-14,7
6-12thn:11,5-15,5
12-18thn:13-16(L);12-16(P)
g/dL
Ht 2thn:33-42 %
Leukosit 2thn:6000-17.500 /μL
Trombosit 150.000-400.000 /μL
MCV 2thn:70-86 fL
MCH 2thn:23-31 pg/sel
MCHC 2thn:30-36 %Hb/sel
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Hipokrom: MCH ˂ normal
Mikrositik: MCV ˂ normal
Hiperkrom: MCH ˃ normal
Makrositik: MCV ˃ normal
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Red Cell MorphologyPenyakit (tambahan)
Hereditary, Lipid
disorders,
splenectomy
Hb C disease, post
splenectomy
Myeloid metaplasia
Uremia, following
heparin injection, def
pyruvate kinase
Thalassemia, anemia
megaloblastic, iron
deficiency
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Stage IronDepletion
I
IronDeficiency
II
IDA
III
IronStore
(Ferritin)
SerumIron Normal
Hb Normal Normal MCV,MCHMCHC
Anemia defisiensi Fe
Penyebab:
Peningkatan kebutuhan (pemakaian Fe , infeksi berulang)
Perdarahan kronik
Asupan diet kurang
Malabsorpsi
Kurangnya cadangan besi (prematur, gemelli, anemia pada ibu hamil)
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46. Hemophilia
Bayi perempuan, usia 4 bulan, perdarahan
Riwayat keluarga +
Hb 11,2; leukosit 7.500; trombosit 300.000; BT 2‘;
PT 12‖; aPTT 70‖
Didiagnosis hemofilia A
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Kaskade koagulasi
aPTT
PT
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47. Congenital Heart Disease
Congenital HD
Acyanotic
With ↑ volumeload:
- ASD
- VSD
- PDA
- Valve
regurgitation
1. Nelson‘s textbook of pediatrics. 18th ed.
2. Pathophysiology of heart disease. 5t ed.
With ↑ pressureload:
- Valve stenosis
- Coarctation ofaorta
Cyanotic
With ↓pulmonary blood
flow:
- ToF
- Atresiapulmonal
- Atresiatricuspid
With ↑pulmonary blood
flow:
- Transpositionof the great
vessels
- Truncusarteriosus
Tekanan di dalam Jantung
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Acyanotic Congenital HD:General Pathophysiology
With↑ volume load
The most common: left to right shunting
Blood back into the lungs
Fluid leaks into the interstitial space &
alveoly
High level of ventricular output ->↑sympathetic nervous system
If left untreated, ↑ volume load willincrease pulmonary vascular resistance
Clinical Findings
e.g. ASD, VSD, PDA
↓ compliance &↑ work of breathing
Pulmonary edema, tachypnea, chest
retraction, wheezing
↑ Heart rate & stroke volume
↑Oxygen consumption -> sweating,irritability, FTT
Remodelling: dilatation & hypertrophy
Eventually leads to EisenmengerSyndrome
1. Nelson‘s textbook of pediatrics. 18th ed.
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Acyanotic Congenital HD:General Pathophysiology
Clinical Findings
Dilatation happened in the later stage
Severe pulmonic stenosis in newborn
right-sided HF (hepatomegaly,peripheral edema)
Severe aortic stenosis left-sided(pulmonary edema, poor perfusion) &
right-sided HF
With↑ pressure load
Obstruction to normal blood flow:pulmonic stenosis, aortic stenosis,
coarctation of aorta.
Hypertrophy & dilatation of ventricularwall
Defect location determine thesymptoms
1. Nelson‘s textbook of pediatrics. 18th ed.
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Cyanotic Congenital HD
The degree of cyanosis depends on:
the degree of obstruction to pulmonary blood flow
If the obstruction is mild:
Cyanosis may be absent at rest
These patient may have hypercyanotic spells during condition of stress
If the obstruction is severe:
Pulmonary blood flow may be dependent on patency of the ductus arteriosus.
When the ductus closes hypoxemia & shock
Cyanotic lesions with ↓ pulmonary blood flow must include both:
an obstruction to pulmonary blood flow & a shunt from R to L
Common lesions:
Tricuspid atresia, ToF, single ventricle with pulmonary stenosis
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Abnormal ventricular-arterialconnections:
- TGA
Total mixing of systemic venous &pulmonary venous within the heart:
- Common atrium or ventricle
- Total anomolous pulmonary venousreturn
Cyanotic Congenital HD
Cyanotic lesions with ↑ pulmonary blood flow is notassociated with obstruction to pulmonary blood flow
Cyanosis is caused by:
- Truncus arteriosus
1. Nelson‘s textbook of pediatrics. 18th ed.
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Ventricular Septal Defect
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VSD:Pathophysiology & Clinical Findings
Ph/: increased of 2nd heart sound
1. Nelson‘s textbook of pediatrics. 18th ed.
Flow across VSD
Over flow across mitral valve
LA, LV, RV volume overload
High systolic pressure & highflow to the lungs pulmonary
hypertension
Pansystolic murmur & thrillover left lower sternum.
If defect is large 3rd heart sound& mid diastolic rumble at the apex.
ECG: Left ventricular hypertrophyor biventricular hypertrophy,
peaked/notched P wave
Ro: gross cardiomegaly
Dyspnea, feeding difficulties, poorgrowth, profuse perspiration,
pneumonia, heart failure.
Duskiness during crying or infection
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VSD:
Pathophysiology & Clinical Findings
cardiomegaly with prominence of
both ventricles,
the left atrium, &
the pulmonary artery.
pulmonary vascular marking
1. Nelson‘s textbook of pediatrics. 18th ed.
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Atrial Septal Defect
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Overflow in the right side ofheart
Enlargement of the RA & RV
Dilatation of the pulmonary artery
The LA may be enlarged
ASD:Pathophysiology & Clinical Findings
The degree of L-to-R shunting is dependent on:
- the size of the defect,
- the relative compliance of the R and L ventricles, &
- the relative vascular resistance in the pulmonary & systemic circulations
Infant has thick & less compliant RV minimal symptoms
As children grow older: subtle failure to thrive, fatigue, dyspneu oneffort, recurrent respiratory tract infection
Pulmonary vascular resistance may begin to increase in adulthood
reversal of the shunt & cyanosis
1. Nelson‘s textbook of pediatrics. 18th ed.
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ASD:Pathophysiology & Clinical Findings
Increased flow into right side ofthe heart & lungs
Constant increased ofventricular diastolic volume
Increased flow across tricuspidvalve
Increased flow acrosspulmonary valve
Ro:
- enlargement of RV, RA, &pulmonary artery
- increased vasvular marking
Wide, fixed 2nd heart soundsplitting
Mid-diastolic murmur at thelower left sternal border
Thrill & systolic ejection murmur, bestheard at left middle & upper sternalborder
Flow across the septal defect doesn’t produce murmur because the pressuregap between LA & RA is not significant
1. Nelson‘s textbook of pediatrics. 18th ed.
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ASD:Pathophysiology & Clinical Findings
size of the main pulmonary
artery
size of the right atrium
size of the right ventricle
(seen best on the lateral view
as soft tissue filling in the lower
& middle retrosternal space).
1. Nelson‘s textbook of pediatrics. 18th ed.
2. Essentials of Radiology. 2nd ed.
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Patent Ductus Arteriosus
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Coarctasio of Aorta
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Tetralogi Fallot
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48.Tropic Infection:
typhoid fever
Etiology:Salmonella typhosa
Clinical features: Step ladder fever in
the first week, thepersist
Abdominal pain
Diarrhea/constipation
Headache
Coated tongue
Hepatosplenomegaly
Rose spot
Harrison‘s principles of internal medicine. 18th ed.
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• Muscle tenderness in the muscles
Tropic Infection: leptospirosis
Infection through themucosa or wounded skin
Proliferate in thebloodstream or
extracellularly within organ
Disseminatehematogenously to all
organs
Multiplication can cause:
• Hepatitis, jaundice, & hemorrhage in the liver• Uremia & bacteriuria in the kidney• Aseptic meningitis in CSF & conjunctival or scleral hemorrhage in the aqueous humor
Harrison‘s principles of internal medicine. 18th ed.
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Lauralee S. Human physiology. From cells to system.
49. Electrolyte: Natrium regulation
Sodium functions:
fluid balance (the major
factor in extracellular
osmolality)
nerve impulse
generation &
transmission
(neuromuscular
function).
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Electrolyte: hyponatremia
Many symptoms of
hyponatremia are associated
with the hypotonic hydration.
The most common symptoms:
• Headache
• Nausea
• Disorientation
• Tiredness
• Muscle cramps
Johnson JY. Fluids and Electrolytes demystified. 2008
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Electrolyte: hyponatremia
Natrium concentration is influenced by the balance of natrium &
water in the body.
Harrison‘s principles of internal medicine. 18th ed.
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Electrolyte: hypernatremia
Hypernatremia can affect
brain cells and cause
neurologic damage,
resulting in
Confusion
Paralysis of the muscles
of the lungs
Coma
Even death
Hypernatremia
Fluid moves out of the cells
Cell dehydration with shrinkage
Dry tissues dry mucous membrane, lossof turgor, & thirst
Johnson JY. Fluids and Electrolytes demystified. 2008