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LO 1: GI BLEEDING

GI BLEEDING Classification -GIB presents as either overt or occult bleeding. -Overt GIB is manifested  by hematemesis, vomitus of red blood or “coffeegrounds” mate- rial; melena, black, tarry, foul-smelling stool; and/or hematochezia, passage of bright red or maroon blood from the rectum. -Occult GIB  may be identified in the absence of overt bleeding when patients pres- ent with symptoms of blood loss or anemia such as lightheadedness, syncope, angina, or dyspnea; or when routine diagnostic evaluation reveals iron deficiency anemia or a positive fecal occult blood test. -GIB is also categorized by the site of bleeding as UGIB, LGIB, or obscure GIB if the source is unclear.

UPPER GI BLEEDING - Definition : Upper GI (UGI) bleeding is any GI bleeding originating proximal to the ligament of Treitz - Etiology : Helicobacter pylori rates, socioeconomic conditions, and prescription patterns of ulcer-healing and ulcer-promoting medications, Increasing age, coexistent organ system disease

UGI BLEEDING - Pathophysiology PEPTIC ULCER DISEASE - peptic ulcer disease, which includes gastric, duodenal, esophageal, and stomal ulcers, is still considered the most common cause of UGI bleeding - E/ : Awareness that aspirin, NSAIDs, and smoking cause bleeding and increased recognition and treatment of H. pylori infection may be responsible for decreased incidence. EROSIVE GASTRITIS AND ESOPHAGITIS - Common predisposing factors include alcohol, salicylates, and NSAIDs. Infection, toxic ingestion, radiation, and stress from severe illness may also cause erosive gastritis. Stress-related mucosal disease occurs in patients with overwhelming sepsis, trauma

ESOPHAGEAL AND GASTRIC VARICES - Esophageal and gastric varices result from portal hypertension and, in the United States, are most often a result of alcoholic liver disease. MALLORY-WEISSSYNDROME - Mallory-Weiss syndrome is bleeding secondary to a longitudinal mucosal tear at the gastroesophageal junction - The classic history is repeated vomiting followed by bright red hematemesis.

Gastric varices • are dilated submucosal veins in the stomach, which can be a lifethreatening cause of bleeding in the upper gastrointestinal tract. • They are most commonly found in patients with portal hypertension, or elevated pressure in the portal vein system,

Peptic ulcer • Starts between meals or during the night • Briefly stops if you eat or take antacids • Lasts for minutes to hours • Comes and goes for several days or weeks

Erosive gastritis

Mallory weiss

• often asymptomatic • characterized by although some complain upper of dyspepsia, nausea, or gastrointestinal vomiting. bleeding • Often, the first sign is secondary to hematemesis, melena, or longitudinal blood in the nasogastric mucosal aspirate, usually within 2 lacerations to 5 days of the inciting (known as event. Mallory-Weiss • Bleeding is usually mild tears) at the to moderate, although it gastroesophagea can be massive if deep l junction or ulceration is present, gastric cardia. particularly in acute stress gastritis.

UGI BLEEDING - DIAGNOSIS HISTORY -Ask about hematemesis, coffee-ground emesis, or melena. Classically, hematemesis and coffee-ground emesis suggest a UGI source. -The presence of melena and age <50 years old more likely indicate an upper GI bleed versus a lower GI bleed, even in patients without hematemesis -Vomiting and retching, followed by hematemesis, suggest a Mallory-Weiss tear. -Review the patient’s medication list carefully  Salicylates, glucocorticoids, NSAIDs, and anticoagulants all place the patient at high risk for GI bleed. -Alcohol abuse is strongly associated with a number of causes of bleeding, including peptic ulcer disease, erosive gastritis, and esophageal varices. -Ingestion of iron or bismuth can simulate melena. -Liquid medications with red dye, as well as certain foods, such as beets, can simulate hematochezia.

PHYSICAL EXAMINATION - Visual inspection of the vomitus for a bloody, maroon, or coffee- ground appearance is the most reliable way to diagnose UGI bleeding in the ED  Consider keeping a sample of the vomitus or nasogastric (NG) aspirate at bedside for the gastroenterologist to view. - Vital signs may reveal obvious hypotension and tachycardia or more subtle findings such as decreased pulse pressure or tachypnea. - Cool, clammy skin is an obvious sign of shock.

LABORATORY TESTING -In patients with significant bleeding, the single most important laboratory test is to obtain blood for type and cross-match in case transfusion is needed. -UGI hemorrhage will elevate BUN levels through digestion and absorption of hemoglobin. A BUN:creatinine ratio ≥30 suggests a UGI source of bleeding.

NASOGASTRIC LAVAGE - NG intubation and aspiration are diagnostic and therapeutic. In patients without a history of hematemesis, a positive aspirate provides strong evidence for a UGI source of bleeding. - Visual inspection of the aspirate for a bloody, maroon, or coffee-ground appearance is the most reliable way to diagnose UGI bleeding in the ED

Tintinalli's Emergency Medicine - A Comprehensive Study Guide 8th 2016.pdf

TREATMENT

Tintinalli's Emergency Medicine - A Comprehensive Study Guide 8th 2016.pdf

(Patient Teaching Guides - Evidence-Based Diagnosis) Fred F. Ferri-Ferri’s Clinical Advisor 2017. 5 vols.-Expert Consult Com. (2017).pdf

Harrison's Principles of Internal Medicine 19th 2015.pdf

Ulcer : -Randomized controlled trials document that high-dose, constant infusion IV proton pump inhibitor (PPI) (80-mg bolus and 8-mg/h infusion), designed to sustain intragastric pH >6 and enhance clot stability, decreases further bleeding and mortality in patients with high-risk ulcers (active bleeding, nonbleeding visible vessel, adherent clot) when given after endoscopic therapy. -Patients with lower-risk findings (flat pigmented spot or clean base) do not require endoscopic therapy and receive standard doses of oral PPI. Mallory weiss tears : -The classic history is vomiting, retching, or coughing preceding hematemesis, especially in an alcoholic patient. Bleeding from these tears, which are usually on the gastric side of the gastroesophageal junction, stops spontaneously in 80–90% of patients and recurs in only 0–10%. Endoscopic therapy is indicated for actively bleeding Mallory-Weiss tears. Angiographic therapy with embolization and operative therapy with oversewing of the tear are rarely required.

Esophageal varices : -Patients with variceal hemorrhage have poorer outcomes than patients with other sources of UGIB. -Urgent endoscopy within 12 h is recommended in cirrhotics with UGIB, and if esophageal varices are present, endoscopic ligation is performed and an IV vasoactive medication (e.g., octreotide 50 μg bolus and 50 μg/h infusion) is given for 2–5 days.

LOWER GI BLEEDING - Lower GI (LGI) bleeding is the loss of blood from the GI tract distal to the ligament of Treitz. - Among patients with an established LGI source of bleeding (i.e., bleeding past the ligament of Treitz), the most common cause is diverticular disease, followed by colitis, adenomatous polyps, and malignancies.

LGI - PATHOPHYSIOLOGY - Hematochezia is either bright red or marooncolored rectal bleeding. If hematochezia originates from a UGI source, it indicates brisk UGI bleed- ing, which may be accompanied by hematemesis and hemodynamic instability. - Melena is dark or black-colored stools and usually represents bleeding from a UGI source

DIVERTICULOSIS - Diverticular bleeding is usually painless and results from erosion into the penetrating artery of the diverticulum. VASCULARECTASIA - Vascular ectasia, which includes arteriovenous malformations and angiodysplasias of the colon, is a common cause of LGI bleeding. ISCHEMIC COLITIS AND MESENTERIC ISCHEMIA - Ischemic colitis is the most common cause of intestinal ischemia and is usually transient. - The colon is predisposed to ischemia because of its poor vascular circulation and high bacterial content. - Aneurysmal rupture, vasculitis, hypercoagulable states, prolonged strenuous exercise, cardiovascular insult, irritable bowel syndrome, and certain medications that cause vasoconstriction or slow bowel motility are known risk factors. - Mesenteric ischemia can lead to bowel necrosis. Causes include thrombosis or embolism of the superior mesenteric artery, mesenteric venous thrombosis, and nonocclusive mesenteric ischemia associated with low arterial flow with vasoconstriction.

MECKEL’SDIVERTICULUM -Meckel’s diverticulum consists of embryonic tissue, most commonly found in the terminal ileum. -More than half of lesions contain ectopic gastric tissue, which can secrete gastric enzymes, eroding the mucosal wall and causing bleeding.

LGI - DIAGNOSIS - Factors associated with a high morbidity rate are hemodynamic instability, repeated hematochezia, gross blood on initial rectal examination, initial hematocrit <35%, syncope, nontender abdomen (predictive of severe bleeding), aspirin or non- steroidal anti-inflammatory drug use (predictive of diverticular hemorrhage),

HISTORY - Although most patients will volunteer complaints of hematochezia or melena, signs and symptoms of hypotension, tachycardia, angina, syncope, weakness, or altered mental status can all occur as a result of LGI bleeding. - Ask about previous GI bleeding as well as a history of pain, trauma, ingestion or insertion of foreign bodies, and recent colonoscopies. - Weight loss and changes in bowel habits may suggest malignancy. - A history of an aortic graft may suggest the possibility of an aortoenteric fistula - Medications, such as salicylates, nonsteroidal anti-inflammatory drugs, and warfarin, increase the risk of LGI bleeding.14-16 Ingestion of iron or bismuth can simulate melena, and certain foods, such as beets, can simulate hematochezia.

PHYSICAL EXAMINATION -Hypotension and tachycardia, or decreased pulse pressure or tachypnea, develop with significant bleeding -However, changes in vital signs may be masked by concurrent medications, such as β-blockers, or medical conditions such as poorly controlled hypertension. -Cool, pale skin and an increase in capillary refill can be signs of shock. -The abdominal examination : disclose tenderness, masses, ascites, or organomegaly -In patients with LGI bleeding, a lack of abdominal tenderness suggests bleeding from disorders involving the vasculature, such as diverticulosis or angiodysplasia. Inflammatory bowel disorders with LGI bleeding are associated with abdominal tenderness on examination.

- Rectal examination : may reveal an obvious source of bleeding, such as a laceration, masses, trauma, anal fissures, or external hemorrhoids - digital rectal examination to detect gross blood (either bright red or maroon) and for guaiac testing. Rectal examination can also detect the presence of masses.

LABORATORY TESTING - The most important laboratory tests are the CBC, coagulation studies, and typed and cross-matched blood - Coagulation studies, including prothrombin time, partial thromboplastin time, and platelet count, are of obvious benefit in patients taking anticoagulants or those with underlying hepatic disease. • Bleeding from a source higher in the GI tract may elevate blood urea nitrogen levels through digestion and absorption of hemoglobin. • Obtain an ECG in patients with coronary artery disease. Silent ischemia can occur secondary to the decreased oxygen delivery accompanying significant GI bleeding.

IMAGING - Angiography can sometimes detect the site of bleeding and help guide surgical management. Moreover, angiography permits therapeutic options such as transcatheter arterial embolization or the infusion of vasoconstrictive agents. - angiographic diagnosis and therapy require a relatively brisk bleeding rate (at least 0.5 mL/ min). Serious complications can also occur with angiography in up to 10% of cases. - Scintigraphy appears more sensitive than angiography and can localize the site of bleeding at as low a rate as 0.1 mL/min. It also has potential value over angiography if bleeding occurs intermittently but requires a minimum of 3 mL of blood to pool. - Multidetector CT angiography has a sensitivity and specificity of up to 100% and 99%, respectively, for detecting active or recent GI bleeding and is about 93% accurate in determining the site of bleeding.23,24 It can be a useful tool prior to treatment with conventional angiography.

TREATMENT -Resuscitate unstable or actively bleeding patients. Administer oxygen and institute cardiac monitoring. Place two large-bore IV lines and replace volume with crystalloids. -Blood transfusion should be based on the clinical findings of volume depletion or continued bleeding rather than on initial hematocrit values. In acute bleeding, hematocrit values may not represent true blood volume status, because it takes several hours for the hematocrit to decrease. -General guidelines for initiation of blood transfusion are continued active bleeding and failure to improve perfusion and vital signs after the infusion of 2 L of crystalloid. -Consider the placement of a nasogastric tube if LGI bleeding is significant. Hematochezia unexpectedly originates from UGI sources approximately 10% to 14% of the time.

LO 2: ACUTE ABDOMEN

Abdominal Pain • Pain with other symptoms that are not typical of any spesific disease process • Emergency condition : – Ederly – Diverticulitis, ruptur abdominal, mesenteric iscchemia – Patients in immunocompromised states

• Gastrointestinal & genitourinary tract are the most common source of pain

Abdominal Pain Abdominal pain is derived from 3 distinct pain pathways : • Visceral • Somatic • Reffered

Abdominal Pain Visceral pain • From stimulating autonomic nerves invested in viseral peritoneum surrounding internal organs • Cause : – Distension by fluid or gas – Capsular stretching of solid organs ( edema, blood, cysts. Abcess )

• Poory characterized and difficult to localize • Corelated with embryonic somatic segments

Abdominal Pain Embryotic somatic segments : • Foregut (stomach, duodenum, liver, pancreas) • Midgut (small bowel, proximal colon, appendix) • Hindgut (distal colon, genitourinary tract)

Abdominal Pain Somatic pain • Occurs with irritation of the parieta peritoneum • Caused by infection, chemical irritation, or another inflammatory process • Sensation conducted by peripheral nerves • Better localized than visceral pain • The pain often described as intense and constant

Abdominal Pain Reffered pain • Pain felt at a distant from its source • Periferal afferent nerve fibers from many organs >> spinal cord >> nociceptive fibers from other location

Differential Diagnosis

Physical Examination • Vital signs ( !!tachycardi, hypotension, tacypnoe!! ) • Elevated temperature • Abdominal examination • Pelvic examination for female • Urogenital examination for male • Pelvic ultrasound for female • CT scan

Management • • • •

Acute = analgesic iv ( ketorolac iv ) GI bleeding ketorolac increase bleeding times Gastric acid = antasid Intestinal cramping = atropine-skopolaminhyosiamin-fenobarbital • Nausea and vomiting = promethazine, ondansetron, granisetron, inapsine • Small bowel obstruction = NGT • Antibiotics

Acute Appendicitis • Acute obstruction of appendiceal lumen • Acute obstruction >> intraluminal pressure rise >> mucosal secretions are unable to drain >> ditension >> viseral afferent pathways >> dull, poorly localized pain >> ulceration & ischemia >> bacteria begin to invade • Hyperperistaltis >> abdominal cramping • Appendix swolen >> irritate surrounding structures >> peritoneum >> localize pain

Acute Appendicitis • • • • •

Dull periumbilical paiin Anorexia, nausea, vomiting Right lower quadrant Increased urinary frequency Desire to defecate

Acute Appendicitis Physical examination • Localized abdominal tenderness • Mcburney’s sign + • Rovsing sign + • Tensing of abdominal wall • Vital sign often normal

Laboratory test • Leukosit count • CRP • Urynalisis • Pregnancy test Imaging • Barium enema • Nuclear imaging • USG • CT/MRI • Laparoscopy

Acute Appendicitis Management • Dehydrated patients = crystaloid fluids • Nausea vomiting = parenteral antiemetic • Surgical =appendyctomy

Acute peritonitis • Definition: Inflammation of the peritoneum, may be localized or diffuse, acute or chronic, infectious or aseptic. • Most often infectious and usually related to a perforated viscus (secondary peritonitis). • When no intraabdominal source is identified, infectious peritonitis is primary or spontaneous. • Associated with decreased intestinal motor activity  distention of the intestinal lumen with gas and fluid  rapid intravascular volume depletion Fauci AS, Braunwald E, Kasper DL, Hauser SL, Longo DL, Jameson JL, et al, editors. Harrison’s principle of internal medicine. 17th ed. USA: McGraw Hill Medical, 2008.

Acute peritonitis • Etiology: – Infectious agents gain access to peritoneal cavity (through perforated viscus or external introduction of infected foreign object): most common conditions are ruptured appendix, ruptured diverticulum, perforated peptic ulcer, incarcerated hernia, gangrenous gall bladder, volvulus, bowel infarction, cancer, inflammatory bowel disease, or intestinal obstruction – Aseptic peritonitis may be due to peritoneal irritation by abnormal presence of physiologic fluids or sterile foreign bodies in the peritoneal cavity or as a complication of rare systemic diseases such as lupus erythematous, porphyria, or familial Mediterranean fever. Fauci AS, Braunwald E, Kasper DL, Hauser SL, Longo DL, Jameson JL, et al, editors. Harrison’s principle of internal medicine. 17th ed. USA: McGraw Hill Medical, 2008.

Acute peritonitis • Clinical features: – Acute abdominal pain and tenderness, usually fever – Location of pain depends on the underlying cause and whether it is localized (most common in uncomplicated appendicitis and diverticulitis) or generalized (associated with widespread inflammation and diffuse abdominal tenderness and rebound). – Rigidity of the abdominal wall – Absent bowel sound – Tachycardia, hypotension, signs of dehydration Fauci AS, Braunwald E, Kasper DL, Hauser SL, Longo DL, Jameson JL, et al, editors. Harrison’s principle of internal medicine. 17th ed. USA: McGraw Hill Medical, 2008.

Acute peritonitis • Examination: – Leukocytosis and marked acidosis – Plain abdominal films show dilataion of large and small bowel with edema of the bowel wall – Free air under diaphragm is associated with a perforated viscus – CT/ ultrasonography can identify the presence of free fluid or an abscess – If ascites (+): diagnostic paracentesis with cell count (>250 neutrophils/μL in usual peritonitis), protein and lactate dehydrogenase leves, and culture is essential

Fauci AS, Braunwald E, Kasper DL, Hauser SL, Longo DL, Jameson JL, et al, editors. Harrison’s principle of internal medicine. 17th ed. USA: McGraw Hill Medical, 2008.

Acute peritonitis • Therapy and prognosis: – Treatment relies on rehydration, correction of electrolyte abnormalities, antibiotics, and surgical correction of the underlying defect. – Mortality rates are <10% for uncomplicated peritonitis associated with a perforated ulcer or ruptured appendix or diverticulum in an otherwise healthy person. – Mortality rates of ≥40% have been reported for elderly people, those with underlying illnesses, and when peritonitis has been present for >48h

Fauci AS, Braunwald E, Kasper DL, Hauser SL, Longo DL, Jameson JL, et al, editors. Harrison’s principle of internal medicine. 17th ed. USA: McGraw Hill Medical, 2008.

Intussusception • Intussusception occurs when a portion of the alimentary tract is telescoped into an adjacent segment. • Epidemiology : – The most common cause of intestinal obstruction between 5 mo and 3 yr of age and the most common abdominal emergency in children younger than 2 yr. – 60% of patients are younger than 1 yr of age, and 80% of the cases occur before age 24 mo; it is rare in neonates. – Male : Female ratio is 3 : 1 Nelson Textbook of Pediatrics 20th ed

Intussusception • Etiology : – 90% of cases of intussusception in children are idiopathic – Correlation with prior or concurrent respiratory adenovirus (type C) infection has been noted – Gastrointestinal infection or the introduction of new food proteins results in swollen Peyer patches in the terminal ileum. Lymphoid nodular hyperplasia is another related risk factor. Prominent mounds of lymph tissue lead to mucosal prolapse of the ileum into the colon, thus causing an intussusception. – Recognizable lead points for the intussusception : Meckel diverticulum, intestinal polyp, neurofibroma, intestinal duplication cysts, inverted appendix stump, leiomyomas, hamartomas, ectopic pancreatic tissue, anastomotic suture line, enterostomy tube, posttransplant lymphoproliferative disease, hemangioma, ormalignant conditions such as lymphoma, or Kaposi sarcoma.

Nelson Textbook of Pediatrics 20th ed

Intussusception • Pathology : – Intussusceptions are most often ileocolic, less commonly cecocolic, and occasionally ileal. – The upper portion of bowel, the intussusceptum, invaginates into the lower, the intussuscipiens, pulling its mesentery along with it into the enveloping loop. – Constriction of the mesentery obstructs venous return  engorgement of the intussusceptum follows, with edema, and bleeding from the mucosa leads to a bloody stool, sometimes containing mucus. – Most intussusceptions do not strangulate the bowel within the 1st 24 hr but can eventuate in intestinal gangrene and shock. Nelson Textbook of Pediatrics 20th ed

Intussusception • Clinical Manifestations : – – – – – – – –

Severe paroxysmal colicky pain Weak, lethargic Shock-like state, with fever and peritonitis Pulse becomes weak and thready, the respirations become shallow and grunting, and the pain may be manifested only by moaning sounds. Vomiting (early phase)  bile stained (later phase) A stool containing red blood and mucus, the currant jelly stool. Palpation of the abdomen usually reveals a slightly tender sausage-shaped mass Rectal examination : bloody mucus Nelson Textbook of Pediatrics 20th ed

Intussusception • Radiology : – Abdominal radiograph (AP and left side down decubitus view) – USG  a “donut sign” or a “pseudokidney sign” – CT scan – Barium enema (not for bowel perforation) – Colonoscopy (defining the lession) The Atlas of Emergency of Radiology

Intussusception • Treatment : – Reduction of an acute intussusception is an emergency procedure and should be performed immediately after diagnosis in preparation for possible surgery. – Optimizing fluid status – In patients with prolonged intussusception and signs of shock, peritoneal irritation, intestinal perforation, or pneumatosis intestinalis, hydrostatic reduction should not be attempted. – Surgical reduction is indicated in the presence of refractory shock, suspected bowel necrosis or perforation, peritonitis, and multiple recurrences (suspected lead point). – If manual operative reduction is impossible or the bowel is not viable, resection of the intussusception is necessary, with endto-end anastomosis. Nelson Textbook of Pediatrics 20th ed

Intussusception • Prognosis : – Untreated intussusception in infants is usually fatal – Most infants recover if the intussusception is reduced in the 1st 24 hr, but the mortality rate rises rapidly after this time, especially after the 2nd day. – The recurrence rate after reduction of intussusceptions is approximately 10%, and after surgical reduction it is 2-5%; none has recurred after surgical resection.

Nelson Textbook of Pediatrics 20th ed

LO 3: SHOCK

Shock • Syndrome that results from inadequate tissue perfusion • Imbalance between delivery of and requirement of oxygen >> cellular disfunction • Cellular injury >> inadequate delivery of oxygen >> inflamatory mediators >> compromise perfusion >> multiple organ failure

Shock Treatment • Monitor : arterial pressure, pulse, respiratory rte, mental status • PAC for shock with blood loss, fluid shifts, cardiac disfunction • Optimize oxygen delivery, hemodynamics, and cardiac function rapidly

Type of Shock

Cardiogenic Shock CLINICAL FINDINGS • Chest pain, dyspnea, pale, apprehensive, diaphoretic • Somnolence, confusion, agitation • Pulse typically weak and rapid: 90–110 beats/min, or severe bradycardia due to high-grade heart block • Systolic blood pressure reduced (<90 mmHg), narrow pulse pressure (<30 mmHg) • Tachypnea, Cheyne-Stokes resp, jugular venous distention • Precordium quiet, with a weak apical pulse • S1 is usually soft, and an S3 gallop may be audible

Harrison’s Principle of Internal Medicine 18th ed

Cardiogenic Shock LABORATORY FINDINGS • WBC elevated with left shift • Blood urea nitrogen and creatinine rise progressively • Hepatic transaminases markedly elevated. • Anion-gap acidosis and elevation of the lactic acid level. • Arterial blood gases: hypoxemia and metabolic acidosis (or compensated: alkalosis) • Cardiac markers, creatine phosphokinase and its MB fraction, and troponins I and T are markedly elevated.

Harrison’s Principle of Internal Medicine 18th ed

Cardiogenic Shock ELECTROCARDIOGRAM • Due to acute MI with LV failure: Q waves and/or >2-mm ST elevation in multiple leads or left bundle branch block • >½ infarcts associated with shock are anterior. • Global ischemia due to severe left main stenosis  severe (e.g., >3 mm) ST depressions in multiple leads.

Harrison’s Principle of Internal Medicine 18th ed

Anafilaksis • Rx hipersensitivitas sistemik/general yang berat dah mengancam nyawa – Dicirikan dengan gangguan A/B/C yang berkembang sangat cepat biasanya akibat perubahan kulit/mukosa (cth: edema)

• Epidemiologi: 1 jt kasus anafilaksis venom & 0.4 jt kasus anafilaksis kacang hingga usia 44 tahun worldwide

Resuscitation Council (UK). Emergency treatment of anaphylactic reactions – Guidelines for healthcare providers. Jan 2008.

Anafilaksis • Anafilaksis = reaksi IgE-mediated • Anafilaktoid = reaksi non–IgE-mediated • Sindrom anafilaksis = tanda gejala klinis

Medscape. Pediatric Anaphylaxis

Anafilaksis • Pencetus: makanan (anak), obat-obatan (dws), bisa (venom)

Resuscitation Council (UK). Emergency treatment of anaphylactic reactions – Guidelines for healthcare providers. Jan 2008.

Anafilaksis • Mortalitas: prognosis keseluruhan baik, fatalitas <1%, peningkatan risiko kematian dengan asma/adrenalin terlambat • Rekurensi cukup besar 1 dari 12 per tahun • Kematian tidak pernah terjadi lewat dari 6 jam pasca terpapar

Resuscitation Council (UK). Emergency treatment of anaphylactic reactions – Guidelines for healthcare providers. Jan 2008.

Patofisiologi Anafilaksis • Anafilaksis: antigen  sel B produksi IgE  sel mast & basofil terpapar ulang  cross-link dg IgE di sel mast & basofil  degranulasi – Perlu ≥2 keterpaparan

• Anafilaktoid: – Administrasi produk darah, IVIg, antiserum hewan  aktivasi kompleks imun (degranulasi C3a, C4a, C5a) – Direct release oleh: opioid, dextrans, protamine, vancomycin  histamin, leukotrien, PG, platelet activating factors

Medscape. Anaphylaxis

Diagnosis Anafilaksis • Terpapar pencetus (alergen)  sakit tiba-tiba (menit)  perubahan kulit cepat & progres gangguan A/B/C • Reaksinya biasa tidak terduga • Tidak ada manifestasi konsisten. Beberapa kombinasi tanda meningkatkan kemungkinan rx anafilaktik • Rx alergi sistemik sulit dibedakan: urtikaria generalisata, angioedema, rhinitis (tanpa gangguan ABC yang mengancam nyawa)

Resuscitation Council (UK). Emergency treatment of anaphylactic reactions – Guidelines for healthcare providers. Jan 2008.

Diagnosis Anafilaksis

Resuscitation Council (UK). Emergency treatment of anaphylactic reactions – Guidelines for healthcare providers. Jan 2008.

Diagnosis Anafilaksis • Gejala mendadak dan progresi cepat: – Terlihat tidak sehat – Reaksi terjadi beberapa menit – Rx IV lebih cepat daripada oral – Terlihat cemas dan merasa “sense of impending doom”

Resuscitation Council (UK). Emergency treatment of anaphylactic reactions – Guidelines for healthcare providers. Jan 2008.

Diagnosis Anafilaksis • Gangguan A/B/C yang mengancam nyawa: – Airway: edema faring/laring  sulit napas/telan, suara serak, stridor, obstruksi – Breathing: sesak napas (takipneu), wheeze, fatigue, hipoksia  confusion, sianosis (late feature), henti napas – Circulation: syok (pucat, akral dingin), takikardia, hipotensi, pusing, kolaps, penurunan kesadaran, MI (EKG meski a. koroner normal), henti jantung Resuscitation Council (UK). Emergency treatment of anaphylactic reactions – Guidelines for healthcare providers. Jan 2008.

Diagnosis Anafilaksis • Gangguan sirkulasi = syok anafilaktik – Akibat depresi miokard, vasodilatasi, bocor kapiler, kehilangan cairan – Bradikardia (late feature)  henti jantung – Respon sementara thd posisi baring & trendelenburg, memburuk bila duduk/berdiri

• Gangguan A/B/C  penurunan perfusi otak  perubahan status neurologis (Disability problems) • Gejala GI: nyeri abdomen, inkontinensia, muntah

Resuscitation Council (UK). Emergency treatment of anaphylactic reactions – Guidelines for healthcare providers. Jan 2008.

Diagnosis Anafilaksis • Perubahan kulit/mukosa (Exposure): – Seringkali merupakan fitur utama, ada pada 80% kasus rx anafilaktik – Ringan hingga berat, hanya kulit/mukosa/keduanya – Eritema, urtikaria, gatal – Angioedema (edema hingga jaringan dalam): kelopak mata, bibir, mulut, tenggorokan

Resuscitation Council (UK). Emergency treatment of anaphylactic reactions – Guidelines for healthcare providers. Jan 2008.

Diagnosis Anafilaksis • Bayi & anak tidak dapat mengekspresikan rasa tidak nyaman (gatal, panas) secara verbal  menangis, muntah persisten, iritabel • Anak tidak dapat mengidentifikasi agen pemicu (cth: makanan)  harus diperhatikan oleh perawat

Medscape. Pediatric Anaphylaxis.

Diagnosis Banding Anafilaksis • Life-threatening: – Asthma berat – Syok septik (TD ↓ + ruam peteki/purpurik)

• Non life-threatening: – Pingsan (episode vasovagal) – Panic attack – Angioedema/urtikaria idiopatik (non-allergic)

Resuscitation Council (UK). Emergency treatment of anaphylactic reactions – Guidelines for healthcare providers. Jan 2008.

Tatalaksana Anafilaksis • Tatalaksana spesifik tergantung: – Lokasi – Kemampuan penolong – Jumlah responder – Peralatan & obat-obatan yg tersedia

Resuscitation Council (UK). Emergency treatment of anaphylactic reactions – Guidelines for healthcare providers. Jan 2008.

Tatalaksana Anafilaksis • • • • • • •

Recognition and early treatment ABCDE approach Adrenaline Investigate Specialist follow up Education – avoid trigger Consider auto-injector

Resuscitation Council (UK). Emergency treatment of anaphylactic reactions – Guidelines for healthcare providers. Jan 2008.

Tatalaksana Anafilaksis • Pasien tanpa gejala yang mengancam nyawa diobservasi 4-6 jam pasca tatalaksana berhasil  pulang • Pasien dengan anafilaksis berat/refrakter (+ gejala KV/respi)  rawat inap, observasi lebih lama di UGD

http://emedicine.medscape.com/article/135065-treatment#d9

Tatalaksana Anafilaksis • Epinefrin IM di vastus lateralis: konsentrasi plasma maksimum lebih tinggi & cepat dibandingkan IM/SC di deltoid

http://emedicine.medscape.com/article/135065-treatment#d9

Resuscitation Council (UK). Emergency treatment of anaphylactic reactions – Guidelines for healthcare providers. Jan 2008.

Resuscitation Council (UK). Emergency treatment of anaphylactic reactions – Guidelines for healthcare providers. Jan 2008.

Hypovolemic Shock • Shock results from the loss of red blood cell mass and plasma from hemorage or loss of plasma volume alone due to extravascular fluid sequestration or GI, urinary, and insensible loss • Sympathetic activity increase, hyperventilation, collapse, release of stress hormones, reduction of urine output

Hypovolemic Shock • Acute haemorrhage >> hematocrit and hemoglobin do not change until compensatory fluid shifts occur • Plasma losses >> free water loss >> hyponatremia

Hypovolemic Shock Treatment • Initial resuscitation • Volume resuscitation with rapid infusion of saline isotonic or ringer lactate • Acute blood loss >> transfusion >> blood volume restored >> inotropic support ( norepinefrin, vasopresin or dopamine )

Neurogenic Shock • Interruption of sympatethic vasomotor input after a high cervical spinal cord injury, spinal anesthesia, davstating head injury • Venodilation >> decreased venous return and cardiaac output • The ectremities often warm • Treatment simultaneous approach to the relative hypovolemia • Norepinefrin or alpha adrenergik agent to augment vascular resistance

• Management: 1. Cristaloid fluid IV for hyotension 2. Atropin for bradikardia 3. Corticosteroid for trauma in spinal cord 4. Consultation to neuron department

Hypoadrenal Shock • Unrecognized adrenal insufficiency complicates the host response to stress induced by acute illness or major surgery • Adrenocortical insufficiency >> high dose of glucokotikoid • Loss of homeostasis with reduction in systemic vascular resitance, hypovolemia, reduced cardiac output • Diagnosis with ACTH stimulation test but inconsistent

Hypoadreal Shock Treatment • Hemodynamicaly patient : dexamethasone sodium phospate 4 mg iv • Non response to ACTH stimulation ( cortisol <9 microgram/dl) >> hydrocortisone 100 mg every 6-8 hours >> tapper down