Blok Kegawatdaruratan 1

FIRST PROBLEM
A Bloody Situation
FORTUNE DE AMOR
405140230
GROUP 8
Peptic Ulcer Disease
Peptic ulcer classically causes epigastric gnawing or burning,

often occurring nocturnally and promptly relieved by food or
antacids
Etiology
 H pylori infection
 Drugs
 Lifestyle factor
Haririson’s Principles of Internal Medicine BS Anand, MD . Peptic Ulcer Disease.
(19 th edition) http://emedicine.medscape.com/article/181753-
overview
(disorder commonly associated with vomiting)
Class Acute Chronic
History Epigastric pain present in 90% of cases. Classically, duodenal ulcer
pain is relieved by food, whereas gastric ulcer pain is made worse.
Presence of severe pain should raise suspicion of perforation.
Prevalance Very common
Physical Mild epigastric tenderness
examination
Useful test Hemoglobin and hemoccult testing if bleeding is suspected
Upright abdominal film if perforation is suspected
Comments Three major causes of PUD are NSAIDs, Helicobacter pylori
infection, and hypersecretory states
Rosen Emergency Medicine
TREATMENT
 PPIs
 H2RAs
 OTHER AGENTS (Sucralfate, Antacids, Misoprostol)
 H. PYLORI ERADICATION (triple therapy” with a PPI, clarithromycin, and
either amoxicillin or metronidazole. In areas where clarithromycin resistance is
high, quadruple therapy or sequential therapy may be the preferred option)
Tintinalli Emergency Medicine

Neurogenic shock
Definition
Acute spinal cord injury cause sympathetic outflow is disrupted leaving unopposed vagal
tone.
Etiology
– Interruption of sympathetic vasomotor input after
• a high cervical spinal cord injury
• inadvertent cephalad migration of spinal anesthesia
• devastating head injury
~Occurs after acute spinal cord injury
–  arteriolar dilation + venodilation  pooling in the venous system  venous return
and cardiac output <
Harrison's principles of internal medicine, 18th

• Signs and symptomps
– Kulit hangat dan kering
– Kecemasan
– Kehilangan kesadaran
– Hipotensi
– Menunjukkan gejala – gejala hipotermia
– Sesak nafas
– Bradikardia
• Treatment
– Excessive volumes of fluid + norepinephrine or a pure -adrenergic
agent (phenylephrine) if hemorrhage has been ruled out
• Complication
– Perkembangan kegagalan organ
– Kematian dini
Hypovolemic shock
Etiology
– loss of red blood cell mass and plasma from hemorrhage
– loss of plasma volume alone due to extravascular fluid sequestration or GI,
urinary, and insensible losses
Diagnosis
– signs of hemodynamic instability + obvious source of volume loss
– Difficult diagnosis if the source of blood loss is occult
• GI tract, or when plasma volume alone is depleted

Hypovolemic shock
Sign & symptoms
Severe  classic signs of shock
• blood pressure declines and becomes unstable even in the supine position
• mental obtundation is an ominous clinical sign

Hypovolemic shock
Treatment
– Volume resuscitation  isotonic saline / Ringer's lactate
 2–3 L of salt solution over 20–30 min
 severe traumatic brain injury (TBI)  small volumes of hypertonic saline
– Continuing acute blood loss + Hb <= 10 g/dL  blood transf
– Administration of fresh-frozen plasma (FFP) and platelets, packed red
blood cells (PRBCs)
– Extreme emergencies  type-specific or O-negative packed red cells
– norepinephrine, vasopressin, or dopamine may be required
• ONLY IF blood volume has been restored
– Supplemental oxygen + intubation

Cardiogenic shock
Cardiogenic shock & pulmonary edema
•  life-threatening conditions that should be treated as
medical emergencies
• Etiology
– severe left ventricular (LV) dysfunction  pulmonary congestion
and/or systemic hypoperfusion

Cardiogenic shock
• systemic hypoperfusion due to severe depression of the cardiac
index [<2.2 (L/min)/m2]
• sustained systolic arterial hypotension (<90 mmHg)
• elevated filling pressure [pulmonary capillary wedge pressure
(PCWP) > 18 mmHg]
• Most common etiologies

– acute myocardial infarction
– cardiomyopathy or myocarditis
– cardiac tamponade

• Other etiologies
– Post cardiac arrest – Refractory sustained
– Refractory sustained tacchyarrhythmias bradyarrhythmias
– Pulmonary embolus – Toxic metabolic
• Beta blocker/CCB overdose
– Severe valvular heart disease
• Severe acidosis & hypoxemia
• Critical aortic / mitral stenosis
• Acute severe aortic / mitral regurgitation

• Incidence
– leading cause of death of patients hospitalized with MI
• LV failure accounts for ~80% of the cases of CS complicating acute MI
– fell from 20% in the 1960s but has plateaued at ~8% for >20 years
– typically associated with ST elevation MI (STEMI)

• Risk factors • Timing
– acute MI – 1/4 of MI patients develop CS rapidly
– older age (within 6 hour of MI onset)
– female sex – 3/4  later on the 1st day
– prior MI – Subsequent onset of CS 
• reinfarction,
– diabetes
• marked infarct expansion,
– anterior MI location
• a mechanical complication
– reinfarction soon after MI

• Clinical findings
– Continuing chest pain & dyspnea – Tachypnea, Cheyne-Stokes
– Pale, apprehensive, diaphoretic respirations
– Altered consciousness – jugular venous distention
– weak and rapid pulse – S1 is usually soft, and an S3 gallop
• 90–110 beats/min
may be audible
– Systolic BP <90 mmHg + narrow pulse – Acute, severe MR and VSR 
pressure (<30 mmHg) systolic murmurs
– quiet precordium + weak apical pulse – LV failure causing CS  rales
– Oliguria
• urine output < 30 mL/h

• Laboratory findings • ECG
– WBC count > with left shift – acute MI with LV failure
– BUN & creatinin >> • Q waves and/or >2-mm ST elevation in
multiple leads
– Hepatic transaminase >>
• LBBB
– Lactic acid >
– 1,5 of infarct  anterior
– Arterial blood gases
– severe left main stenosis  global
• hypoxemia and metabolic acidosis
ischemia
– creatine phosphokinase, troponin I • severe (e.g., >3 mm) ST depressions in
&T> multiple leads

• Chest X ray • Echocardiogram
– pulmonary vascular – left-to-right shunt in patients
congestion with VSR
– pulmonary edema – Pulmonary embolism 
– CS results from a first MI Proximal aortic dissection with
 heart’s size is normal aortic regurgitation or
tamponade

• Pulmonary artery catheterization

• Prognosis
– wide range of expected death rates
• age, severity of hemodynamic abnormalities, severity of the clinical
manifestations of hypoperfusion, and the performance of early
revascularization
– Independent risk factors
• advanced age; depressed cardiac index, ejection fraction, and BP; more
extensive coronary artery disease; and renal insufficiency

Sepsis & septic shock
SIRS
– 2/more of
 fever (oral temperature >38°C) or hypothermia (<36°C)
 tachypnea (>24 breaths/min)
 tachycardia (heart rate >90 beats/min)
 leukocytosis (>12,000/L), leucopenia (<4,000/L)
Sepsis
– SIRS that has a proven or suspected microbial etiology
Septic shock
– Sepsis with hypotension (arterial blood pressure <90 mmHg systolic, or 40 mmHg
less than patient's normal blood pressure) for at least 1 h despite adequate fluid
resuscitation

Nelson’s pediatric, 19th edition
Etiology

Clinical manifestations
 Hyperventilation
 Disorientation, confusion, and other manifestations of encephalopathy
in the elderly and in individuals with preexisting neurologic impairment
 Cellulitis, pustules, bullae, or hemorrhagic lesions
develop when hematogenous bacteria or fungi seed the skin or underlying soft
tissue/the effect of bacterial toxins
 Hypotension and DIC predispose to acrocyanosis and ischemic
necrosis of peripheral tissues
 nausea, vomiting, diarrhea, and ileus  acute gastroenteritis
Clinical manifestations in children
– Primary
 fever, hyperventilation, tachycardia, hypothermia
 cutaneous lesions
o petechiae, ecchymoses, ecthyma gangrenosum, diffuse erythema
 changes in mental status
o confusion, agitation, anxiety, excitation, lethargy, obtundation, or coma
– Secondary
 hypotension, cyanosis
 symmetric peripheral gangrene (purpura fulminans)
 oliguria or anuria
 jaundice (direct hyperbilirubinemia)
 Signs of heart failure
– evidence of focal infection such as meningitis, pneumonia, arthritis, cellulitis, or pyelonephritis
Nelson’s pediatric, 19th edition
Laboratory findings
– Blood lactate levels > early
  accumulation of lactate  metabolic acidosis (with increased anion gap)
 increased glycolysis
 impaired clearance of the resulting lactate and pyruvate by the liver and kidneys
– blood glucose concentration >
 Patients with DM
– Hypoglicemia
 impaired gluconeogenesis
 excessive insulin release on occasion
– Cytokine acute phase response
 inhibits the synthesis of transthyretin
 C-reactive protein, fibrinogen, and complement components >

– leukocytosis with a left shift, thrombocytopenia, hyperbilirubinemia,

and proteinuria
– thrombocytopenia worsens
 prolongation of the thrombin time, decreased fibrinogen, and the presence of
d-dimers  suggesting DIC
– levels of aminotransferases >, azotemia and hyperbilirubinemia
become more prominent
– Hyperventilation  respiratory alkalosis

Other examinations
– Chest radiograph
 normal or may show evidence of underlying pneumonia, volume overload, or
the diffuse infiltrates of ARDS
– ECG
 Tachycardia & nonspecific ST–T-wave abnormalities

Major complications
– Cardiopulmonary
 Ventilation-perfusion mismatching  fall in arterial PO2 early
 generalized maldistribution of blood flow and blood volume and from
hypovolemia  Sepsis-induced hypotension
 Depression of myocardial function
– Adrenal insufficiency
 hypotension that is refractory to fluid replacement and requires pressor therapy
– Renal complications
 Oliguria, azotemia, proteinuria, and nonspecific urinary casts
– Coagulopathy
 Thrombocytopenia & DIC Harrison's principles of internal medicine, 18th
– Neurologic complications
Treatment
– Antimicrobial agents

– Removal of the source of infections

 lungs, abdomen, and urinary tract
 Indwelling IV or arterial catheters should be removed
– Hemodynamic, Respiratory, and Metabolic Support
 IV fluids  1–2 L of normal saline over 1–2 h
 central venous pressure should be maintained at 8–12 cmH2O  avoid pulmonary
edema
 urine output (kept at >0.5 mL/kg per hour) with fluid administration
 mean arterial blood pressure of >65 mmHg (systolic pressure >90 mmHg)
 Ventilator therapy
If hypoxemia, hypercapnia, neurologic deterioration, or respiratory muscle failure
 Erythrocyte transfusion if blood hemoglobin level <= 7 g/dL

– General support
 nutritional supplementation
 reduce the impact of protein hypercatabolism
 Prophylactic heparinization to prevent deep venous thrombosis
 If not have active bleeding or coagulopathy
 tight control of the blood glucose concentration in recovery from critical
illness
 insulin only if it is needed to maintain the blood glucose concentration below 150 mg/dL
 must be monitored frequently (every 1–2 h) for hypoglycemia

Prognosis Prevention
– 20–35% of patients with severe sepsis and – Most are
40–60% of patients with septic shock die
complications of
within 30 days
nosocomial infections
– Others die within the ensuing 6 months
 reducing the number
 result from poorly controlled infection, of invasive procedures
immunosuppression, complications of undertaken
intensive care, failure of multiple
 limiting the use (and
organs, or the patient's underlying
duration of use) of
disease indwelling vascular
and bladder catheters
Anaphylaxis shock
 life-threatening response of a sensitized human appears within
minutes after systemic exposure to specific antigen
intense bronchospasm, vascular collapse, & shock
Cutaneous manifestations
 pruritus and urticaria with or without angioedema
GI manifestations
 nausea, vomiting, crampy abdominal pain, and diarrhea

Anaphylaxis shock
Etiology
antibiotics
 penicillins, cephalosporins, amphotericin B, nitrofurantoin, quinolones
pollen extracts
 ragweed, grass, trees
nonpollen allergen extracts
 dust mites, dander of cats, dogs, horses, and laboratory animals
Food
 peanuts, milk, eggs, seafood, nuts, grains, beans, gelatin in capsules
occupation-related products (latex rubber products)

Anaphylaxis shock
Pathophysiology & manifestations
differ in the time of appearance of symptoms and signs
 hallmark of the anaphylactic reaction is the onset of some manifestation within
seconds to minutes after introduction
Laryngeal edema
 "lump" in the throat, hoarseness, or stridor
 feeling of tightness in the chest and/or audible wheezing (bronchial obstruction)
 Secretions >, peribronchial congestion, submucosal edema, and eosinophilic
infiltration, and the acute emphysema (severe cases)
diffuse erythema and a feeling of warmth
Urticarial eruption + pruritus

Anaphylaxis shock
Diagnosis
onset of symptoms and signs within minutes after the responsible
material is encountered
immunoassays using purified antigens
 presence of specific IgE in the serum of patients with anaphylactic reactions
intracutaneous skin testing
 elicit a local wheal and flare in response to the putative antigen
mast cell activation in a systemic reaction  tryptase levels in serum
>

Anaphylaxis shock
Treatment
0.3 to 0.5 mL of 1:1000 (1 mg/mL) epinephrine SC or IM
 repeated doses as required at 5- to 20-min intervals for a severe reaction
if intractable hypotension occurs
 2.5 mL epinephrine, diluted 1:10,000, at 5- to 10-min intervals IV infusion + normal
saline + vasopressor agents (dopamine)
If hypoxia develops
 Oxygen alone via a nasal catheter or with nebulized albuterol + endotracheal
intubation or a tracheostomy
Ancillary agents
 antihistamine diphenhydramine, 50-100 mg IM or IV
 aminophylline, 0.25-0.5 g IV

Acute Appendicitis
Appendicitis is a very common cause of emergency surgery.
The problem most often occurs when the appendix becomes
blocked by feces, a foreign object, or rarely, a tumor
https://www.nlm.nih.gov/medlineplus/ency/article/000256.htm
ETIOLOGY
 Tumor
 Calculus (often called a stone, is a concretion of material, usually mineral salts,
that forms in an organ or duct of the body)
 Parasite
 Bacteria
 Viral infection
 Enlarged lymph node
 Foreign objects
Harrison_s - Medicina Interna - 16th_Edition

Rosen’s Emergency Medicine Conceps and Clinical Practice
https://www.nlm.nih.gov/medlineplus/ency/article/000256.htm
PATHOPHYSIOLOGY
Obstruction of the appendiceal lumen  intraluminal pressure rise and mucosal
secretions are unable to drain  ulceration and ischemia  bacteria and PMN
cells begin to invade the appendiceal wall  swollen irritate surrounding
structures  hypoxia  gangrene perforation

SIGN & SYMPTOMS
 Abdominal pain (right lower quadrant)
 Anorexia
 Nausea
 Vomiting
 Diarrhea
 Temperature normal or slightly elevated 370C-380C
 Temperature >380C  should suggest perforation
 Leukocytosis (10.000 – 18.000 cells/microL)
 Leukocytosis (>20.000 cells/microL)  suggests probable perforation

Physical examination Diagnostic score
Rovsing’s sign Alvarado score
McBurney’s sign Imaging
Blumberg’s sign Plain radiography
Psoas sign Barium Enema
Obturator sign USG
Lab CT
 Leukocytosis MRI
 CRP Laparoscopy
 Urinalysis

TREATMENT
Early operation and appendectomy as soon as the patient can be
prepared
Cathartics and enemas should be avoided
Antibiotic should not be administered when the diagnosis is in
question

Peritonitis
Peritonitis is an inflammation of the peritoneum, the tissue that lines the inner wall
of the abdomen and covers and supports most of your abdominal organs.
ETIOLOGY
 primary spontaneous peritonitis
An infection that develops in the peritoneum
 secondary peritonitis
usually develops when an injury or infection in the abdominal cavity allows
infectious organisms into the peritoneum.
http://www.webmd.com/digestive-disorders/peritonitis-symptoms-causes-treatments
THE MOST COMMON RISK FACTORS FOR PRIMARY SPONTANEOUS
PERITONITIS INCLUDE:
 Liver disease with cirrhosis
Such disease often causes a buildup of abdominal fluid (ascites) that can become infected.
 Kidney failure getting peritoneal dialysis
The implantation of a catheter into the peritoneum, is used to remove waste products in
the blood of people with kidney failure. It's linked to a higher risk of peritonitis due to
accidental contamination of the peritoneum by way of the catheter.
COMMON CAUSES OF SECONDARY PERITONITIS INCLUDE:
 A ruptured appendix, diverticulum, or stomach ulcer
 Digestive diseases such as Crohn's disease and diverticulitis
 Pancreatitis
 Pelvic inflammatory disease
 Perforations of the stomach, intestine, gallbladder, or appendix
 Surgery
 Trauma to the abdomen, such as an injury from a knife or gunshot wound
• Aseptic peritonitis may be due to peritoneal irritation by
abnormal presence of physiologic fluids (gastric juice, bile,
pancreatic enzymes, blood, urine) or sterile foreign bodies
(surgical sponge, starch from surgical gloves)

SIGN AND SYMPTOMS
 The first symptoms of peritonitis are typically poor appetite and nausea and a dull
abdominal ache that quickly turns into persistent, severe abdominal pain, which is
worsened by any movement.
 Abdominal tenderness or distention
 Chills
 Fever
 Fluid in the abdomen
 Extreme thirst
 Not passing any urine, or passing significantly less urine than usual
 Difficulty passing gas or having a bowel movement
 Vomiting
TEST & DIAGNOSIS
 Blood tests. A sample of your blood may be drawn and sent to a lab to check for a high
white blood cell count. A blood culture also may be performed to determine if there are
bacteria in your blood.
 Imaging tests. Your doctor may want to use an X-ray to check for holes or other
perforations in your gastrointestinal tract. Ultrasound may also be used. In some cases,
your doctor may use a computerized tomography (CT) scan instead of an X-ray.
 Peritoneal fluid analysis. Using a thin needle, your doctor may take a sample of the
fluid in your peritoneum (paracentesis), especially if you receive peritoneal dialysis or
have fluid in your abdomen from liver disease. If you have peritonitis, examination of
this fluid may show an increased white blood cell count, which typically indicates an
infection or inflammation. A culture of the fluid may also reveal the presence of bacteria.
http://www.mayoclinic.org/diseases-conditions/peritonitis/basics/tests-diagnosis/con-20032165
TREATMENT
May need to be hospitalized for peritonitis that's caused by infection from other medical
conditions (secondary peritonitis). Treatment may include:
 Antibiotics. You'll likely be given a course of antibiotic medication to fight the
infection and prevent it from spreading. The type and duration of your antibiotic therapy
depend on the severity of your condition and the kind of peritonitis you have.
 Surgery. Surgical treatment is often necessary to remove infected tissue, treat the
underlying cause of the infection, and prevent the infection from spreading, especially if
peritonitis is due to a ruptured appendix, stomach or colon.
 Other treatments. Depending on your signs and symptoms, your treatment while in the
hospital may include pain medications, intravenous (IV) fluids, supplemental oxygen
and, in some cases, a blood transfusion.
http://www.mayoclinic.org/diseases-conditions/peritonitis/basics/tests-diagnosis/con-20032165
Hernia
 Hernia is defined as an abnormal protrusion of an organ or tissue through a defect
in its surrounding walls
 Abdominal wall hernias occur only at sites at which the aponeurosis and fascia
are not covered by striated muscle
Townsend CM, Beauchamp RD,

Evers BM, Mattox KL. Sabiston
textbook of surgery. 19th Ed.
Philadelphia : Elsevier Saunders;
2012
Incarcerated Hernia
 A hernia is reducible when its contents can be replaced within the surrounding
musculature, and it is irreducible or incarcerated when it cannot be reduced
 If the omentum or a loop of intestine becomes trapped in the weak point in the
abdominal wall, it can obstruct the bowel
 Clinical presentation :
 Severe pain
 Nausea
 Vomiting
 Inability to have a bowel movement or pass gas
 The overlying skin should appear to be normal
 The contents should not be tense
 Bowel sounds can sometimes be heard
Townsend CM, Beauchamp RD, Evers BM, Mattox KL. Sabiston textbook of surgery. 19th Ed. Philadelphia : Elsevier Saunders;
2012
Strangulated Hernia
Strangulation occurs more often in large hernias that have small orifices  entraps
the hernia contents  obstructs arterial blood flow, venous drainage, or both to the
contents of the hernia sac
2012
Strangulated Hernia
Strangulated Hernia
 This can lead to the death of the affected bowel tissue
 Femoral hernias have the highest rate of strangulation
 Clinical presentation :
Hernia associated with
 Vomiting
 Blood in excrement
 Constipation
 Malaise with or without fever
 A burning or hot sensation around the hernia
2012
Management
 Preperitoneal repair
 The hernia sac contents can be directly visualized and their viability assessed
through a single incision
 The constricting ring is identified and can be incised to reduce the entrapped
viscus with minimal danger to the surrounding organs, blood vessels, and nerves
 If it is necessary to resect strangulated intestine, the peritoneum can be opened
and resection done without the need for a second incision.
2012
Complication
If strangulation is not recognized, gangrenous bowel can be
reduced, which leads to peritonitis and sepsis
Recurrent Hernia
Prevention
Hernia should be repaired at the time of discovery
2012
Intussusception
• Invagination of one portion of the bowel

into an immediately adjacent portion
• The proximal segment, or
intussusceptum, is carried by
progressive smooth muscle contractions
into the distal segment, or
intussuscipiens
Source: Sands DR. Intestinal intussusception [Internet]. Clin Colon

Rectal Surg. 2008 May; 21(2): 106–113. Available from:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2780199/
Intussusception may occur anywhere in the small or large
intestine
Nomenclature reflects location in the bowel: enteroenteric,
appendiceal, appendiceal-ileocolic, ileocolic, colocolic,
rectoanal, and stomal

Etiology (pediatric)

Etiology (adult)

CLINICAL PRESENTATION (PEDIATRIC)
 Sudden onset of abdominal pain exhibited by the drawing up of the knees,
screaming, and lethargy between painful bouts
 The onset of pain is shortly followed by obstructive symptoms such as bilious
vomiting and abdominal distension
 Half of cases progress to bloody, mucoid “currant jelly” stools within 12 hours
 Depending on timing of presentation they may or may not have fever and
leukocytosis
 Physical exam  Dance's sign

CLINICAL PRESENTATION (ADULT)
 Abdominal pain
 Nausea/vomiting
 Diarrhea/constipation
 Rectal bleeding
 Common physical findings  distension, hypoactive bowels, abdominal
tenderness, and guaiac positive stools
 Abdominal mass is identified infrequently

TREATMENT (PEDIATRIC)
 Barium suspension with air under fluoroscopic guidance, or
saline plus/minus soluble contrast media under sonographic
guidance
TREATMENT
 Water-soluble contrast agents
 For all patients who
 Pneumatic reduction
present with signs of
perforation, shock, or
peritonitis, immediate TREATMENT (ADULT)
laparotomy is necessary  Definitive surgical intervention is mandatory and
preoperative reduction with barium or air is not
 In the absence of these
recommended as a part of definitive treatment
signs, the therapeutic
 Resect the intussusception en bloc and reduce the
approach to pediatric
intussusception
and adult intussusception
 En bloc resection of all colonic lesions, due to the higher rate
is different
of malignancy, but a more limited resection of small bowel,
where malignancy is less common
Source: Sands DR. Intestinal intussusception [Internet]. Clin Colon Rectal Surg. 2008 May; 21(2): 106–113. Available from:

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FIRST PROBLEM

Peptic ulcer classically causes epigastric gnawing or burning,

Tintinalli Emergency Medicine

Harrison's principles of internal medicine, 18th

Harrison's principles of internal medicine, 18th

Harrison's principles of internal medicine, 18th

Harrison's principles of internal medicine, 18th

Harrison's principles of internal medicine, 18th

• Most common etiologies

Harrison's principles of internal medicine, 18th

Harrison's principles of internal medicine, 18th

Harrison's principles of internal medicine, 18th

Harrison's principles of internal medicine, 18th

Harrison's principles of internal medicine, 18th

Harrison's principles of internal medicine, 18th

Harrison's principles of internal medicine, 18th

Harrison's principles of internal medicine, 18th

Harrison's principles of internal medicine, 18th

Harrison's principles of internal medicine, 18th

Harrison's principles of internal medicine, 18th

Harrison's principles of internal medicine, 18th

– leukocytosis with a left shift, thrombocytopenia, hyperbilirubinemia,

Harrison's principles of internal medicine, 18th

Harrison's principles of internal medicine, 18th

Harrison's principles of internal medicine, 18th

– Removal of the source of infections

Harrison's principles of internal medicine, 18th

Harrison's principles of internal medicine, 18th

Harrison's principles of internal medicine, 18th

Harrison's principles of internal medicine, 18th

Harrison's principles of internal medicine, 18th

Harrison's principles of internal medicine, 18th

Harrison's principles of internal medicine, 18th

Harrison_s - Medicina Interna - 16th_Edition

Rosen’s Emergency Medicine Conceps and Clinical Practice

Harrison_s - Medicina Interna - 16th_Edition

Rosen’s Emergency Medicine Conceps and Clinical Practice

Harrison_s - Medicina Interna - 16th_Edition

Harrison_s - Medicina Interna - 16th_Edition

Townsend CM, Beauchamp RD,

• Invagination of one portion of the bowel

Source: Sands DR. Intestinal intussusception [Internet]. Clin Colon

Source: Sands DR. Intestinal intussusception [Internet]. Clin Colon

Source: Sands DR. Intestinal intussusception [Internet]. Clin Colon

Source: Sands DR. Intestinal intussusception [Internet]. Clin Colon

Source: Sands DR. Intestinal intussusception [Internet]. Clin Colon

Source: Sands DR. Intestinal intussusception [Internet]. Clin Colon

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