SKENARIO 1

BLOK KEGAWATDARURATAN
2011

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Aduh...pahaku sakit sekali...!!!
Seorang laki2 usia 30 tahun dibawa oleh ambulans
puskesmas Bumiaji ke UGD UMM Hospital sambil merintih
kesakitan di paha kanannya. Dari anamnesa singkat oleh
dokter jaga UGD diperoleh keterangan bahwa 2 jam SMRS
saat pasien naik sepeda motor, kecepatan tinggi, dan
memakai helm, tiba – tiba tergelincir dan jatuh ke tepi jalan
sehingga paha kanannya menghantam pembatas jalan.
Riwayat pingsan (-), mual dan muntah (-), GCS 15, tensi
80/40 mmHg, nadi 120x/menit, Respiratory rate 28x/menit,
akral dingin-basah-pucat, deformitas femur dekstra (+), 1/3
tengah femur dekstra terdapat vulnus laceratum ukuran
3x1 cm dengan perdarahan merembes pada kassa
penutup luka, capillary refill 4 detik, nyeri tekan (++)
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Clue and Cue












Laki – laki, 30 thn
Kecelakaan lalulintas
Paha kanan menghantam pembatas jalan
Pingsan –
Mual muntah –
GCS 15
Vital sign :
– Tensi 80/40 mmHg
– Nadi 120x/menit
– RR 28x/menit
Akral dingin-basah-pucat
Deformitas femur dextra +
Shortening ekstrimitas inferior dextra +
Vulnus laceratum 3x1 di 1/3 femur dextra
Darah merembes ke kain kasa
Capillary refill 4 sec
Nyeri tekan ++

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KEYWORD • SYOK (+) 4 .

KLARIFIKASI ISTILAH • • • • Vulnus laceratum : Deformitas : Shortening : Capillary refill : pengisian kembali kapiler >2 sec = shock 5 .

4. – – – – – – 2. 3. mual. Akral dingin-basah-pucat Nadi 120x/menit TD 80/40 mmHg Capillary refill 4 detik Nyeri tekan (++) Pingsan. 5. 6.RUMUSAN MASALAH Apa penyebab pasien mengalami : 1. & muntah (-) Mengapa pasien mengalami syok tetapi GCS dalam batas normal? Apa penyebab adanya deformitas femur dextra? Apa penyebab shortening ekstrimitas inferior dextra? Adakah hubungan antara lamanya pemberian pertolongan dengan timbulnya gejala syok pada pasien? Adakah hubungan antara gejala syok pasien dengan perdarahan akibat vulnus laceratum? 6 .

Apakah diagnosis sementara pada pasien tersebut? Apa saja kemungkinan diagnosa banding pada pasien tersebut? Bagaimanakah penatalaksanaan awal yang dapat dilakukan pada pasien tersebut? Bagaimana terapi dan monitoring pada pasien tersebut? Apa saja komplikasi yang dapat timbul pada pasien tersebut? Bagaimana KIE yang perlu disampaikan pada pasien dan keluarga ttg keadaan pasien? Bagaimana gambaran prognosisnya? 7 . 13. 10.. 7. 9.. 11. 8. 12.LANJUTAN.

Mengapa pasien mengalami syok tetapi 2. Penyebab pasien mengalami : HIPOTESA 1. & muntah (-) . sbg akibat dari pe↓ vol. 2. & muntah (-) – Akral dingin-basah-pucat . (CO = HR X SV) sbg mekanisme kompensasi tubuh untuk mempertahankan CO sehingga perfusi jar. krn adanya hipoperfusi jaringan ekstrimitas atas-bawah – Nadi me↑ .1. Apa penyebab mengalami : – – – – – – pasien Akral dingin-basah-pucat Nadi 120x/menit TD 80/40 mmHg Capillary refill 4 detik Nyeri tekan (++) Pingsan. Adanya fraktur/dislokasi atau kedua2nya 4. Tetap adekuat. krn adanya proses inflamasi – Pingsan. mual. ekstrimitas inferior dextra? 8 . krn adanya hipoperfusi jar. Apa penyebab shortening 4. Darah→venous return ↓ → SV ↓ → CO ↓ = TD ↓ (TD = CO X TPR) – Capillary refill 4 detik. – Nyeri tekan. Diduga tidak terjadi gangguan pada SSP GCS dalam batas normal? secara langsung (head injury) maupun tidak langsung (akibat dari syok yg 3. diduga tidak mengalami trauma kepala. – TD 80/40 mmHg . Apa penyebab adanya ringan) → GCS normal deformitas femur dextra? 3. mual.

Bagaimana KIE yang perlu disampaikan pada pasien dan keluarga ttg keadaan pasien? 9 13. Bagaimana terapi dan monitoring pada pasien tersebut? 11. Apa saja komplikasi yang dapat timbul pada pasien tersebut? 12. Adakah hubungan antara gejala syok pasien dengan perdarahan akibat vulnus laceratum? 7. Bagaimana gambaran prognosisnya? .5. Adakah hubungan antara lamanya pemberian pertolongan dengan timbulnya gejala syok pada pasien? 6. Apa saja kemungkinan diagnosa banding pada pasien tersebut? 9. Apakah diagnosis sementara pada pasien tersebut? 8. Bagaimanakah penatalaksanaan awal yang dapat dilakukan pada pasien tersebut? 10.

Definisi. diagnosis banding. diagnosis. manifestasi klinis. Klasifikasi syok 3.LEARNING OBJECTIVE 1. patofisiologi. Anatomi tulang 2. etiologi. komplikasi. monitoring. penatalaksanaan-terapi-rehabilitasi. dan prognosis dari : 10 . epidemiologi.

1st Learning Object: Anatomy & Compartment of Femur .

Regio Regio Extremitas Inferior. • • • • Regio glutea Regio femoris Regio Cruris Regio pedis .

..Long bone..

Regio Femoris .

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Klasifikasi Shock ( Menurut Hinshaw and Cox classification) .

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ETIOLOGI .

Shock Ischemic Cellular Damage Organ Failure Death .

Septic Shock Cardiogenic Shock Hypovolemic Shock Capillary Leak  Preload Myocardial Depression Mediators  Contractility Vasodilatation  Cardiac Output  Blood Pressure Sympathetic Discharge Improved Cardiac output and blood pressure COMPENSATED Vasoconstriction.   HR  Contractility .

Vasoconstriction  HR  Contractility COMPENSATED DECOMPENSATED DECOMPENSATED  Myocardial perfusion  Myocardial O22 Consumption  Cardiac Output Tissue Ischemia Mediator Release Loss of Auto regulation of Microcirculation  Cell Function Cell Death Death of Organism .

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 Mild ( < 20% blood volume ) ◦ ◦ ◦ ◦ ◦  Ekstremitas terasa dingin Peningkatan capillary refill Diaforesis Vena kolaps Anxiety Moderateural (20-40% blood volume) ◦ Takikardi ◦ Takipneua ◦ Oligouri  Severe ( > 40% blood volume ) ◦ ◦ ◦ ◦ Hemodynamic instability Marked tachycardia Hypotension Coma .

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Etiology & Hemodynamic Changes in Shock Etiology of shock Example CVP CO SVR VO2 sat preload hypovolemic low low high low contractility cardiogenic high low high low afterload distributive .

Etiology & Hemodynamic Changes in Shock (Afterload) ETIOLOGY OF SHOCK EXAMPLE CVP CO SVR VO2 SAT AFTERLOAD DISTRIBUTIVE Hyperdynamic Septic Low/High High Low High Hypodynamic Septic Low/High Low High Low/High Neurogenic Low Low Low Low Anaphylactic Low Low Low Low .

TRAUMA dan SYOK .

Trauma  Keadaan yang menyebabkan luka/injury Gangguan Gangguan  Anatomi / Organ   fisiologis tubuh .

2002.W.METABOLIC RESPONSE TO INJURY (CUTHBERTSON) EBB PHASE  CATHECOLAMINES ELEVATED  GLUCAGON ELEVATED  INSULIN CONCENTRATION LOW  MEDIATED BY CENTRAL NERVE SYSTEM FLOW PHASE  CATHECOLAMINES HIGH NORMAL/ ELEVATED  GLUCAGON ELEVATED  INSULIN CONCENTRATION LOW OR ELEVATED  MEDIATED BY CENTRAL NERVE SYSTEM AND CYTOKINES Wilmore D. Ann of Surg.236(5):643-648 .

W. 2002.236(5):643-648 . Ann of Surg.METABOLIC RESPONSE TO INJURY (CUTHBERTSON) EBB PHASE HYPOMETABOLIC  DECREASE ENERGY EXPENDITURE  EXTREMITIES COLD AND CLAMMY  CARDIAC OUTPUT BELOW NORMAL  CORE TEMPERATURE LOW  NORMAL GLUCOSA PRODUCTION  BLOOD GLUCOSE ELEVATED  FLOW PHASE HYPERMETABOLIC INCREASE ENERGY EXPENDITURE  EXTREMITIES WARM   CARDIAC OUTPUT INCREASE  CORE TEMPERATURE ELEVATED  INCREASE GLUCOSA PRODUCTION  BLOOD GLUCOSE NORMAL / SLIGHTLY ELEVATED  Wilmore D.

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Shock adalah suatu sindroma klinis yg ditandai dg kegagalan sistem sirkulasi untuk mempertahankan perfusi yg adekuat ke organ-organ vital tubuh .

Klasifikasi Shock ( Menurut Hinshaw and Cox classification) .

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ETIOLOGI

Clinical Markers of Shock
• 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;
• Cutaneous vasoconstriction vs. vasodilation.
• Mental Changes: anxiousness, agitation, indifference,
lethargy, obtundation

Shock

Ischemic Cellular Damage

Organ Failure

Death

Septic Shock Cardiogenic Shock Hypovolemic Shock Capillary Leak  Preload Myocardial Depression Mediators  Contractility Vasodilatation  Cardiac Output  Blood Pressure Sympathetic Discharge Improved Cardiac output and blood pressure COMPENSATED Vasoconstriction.   HR  Contractility .

Vasoconstriction  HR  Contractility COMPENSATED DECOMPENSATED DECOMPENSATED  Myocardial perfusion  Myocardial O22 Consumption  Cardiac Output Tissue Ischemia Mediator Release Loss of Auto regulation of Microcirculation  Cell Function Cell Death Death of Organism .

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 Mild ( < 20% blood volume ) ◦ ◦ ◦ ◦ ◦  Ekstremitas terasa dingin Peningkatan capillary refill Diaforesis Vena kolaps Anxiety Moderateural (20-40% blood volume) ◦ Takikardi ◦ Takipneua ◦ Oligouri  Severe ( > 40% blood volume ) ◦ ◦ ◦ ◦ Hemodynamic instability Marked tachycardia Hypotension Coma .

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.Cardiogenic Shock The heart cannot pump enough blood to meet the metabolic demands of the body.

 Loss of contractility: ◦ AMI ◦ Loss of critical mass of left ventricle ◦ RV pump failure ◦ LV aneurysm ◦ End-stage cardiomyopathy ◦ Myocardial contusion ◦ Acute myocarditis ◦ Toxic global LV dysfunction ◦ Dysrhythmias/heart blocks Cardiogenic Shock  Mechanical impairment of blood flow: ◦ Valvular disease ◦ Aortic dissection ◦ Ventricular septal wall rupture ◦ Massive pulmonary embolus ◦ Pericardial tamponade .

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Form of distributive shock. .Neurogenic Shock Spinal cord injury Spinal anesthetic Interruption in the CNS connections with the periphery (spinal cord injury).

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 The skin is warm and dry or a clear sweat line exists. above which the skin is diaphoretic.  Priapism due to Peripheral nervous system stimulation  .Neurogenic shock… As with hypovolemic shock but in high spinal injuries may also be accompanied by profound bradycardia due to loss of the cardiac accelerating nerve fibres from the sympathetic nervous system at T1-T4.

Anaphylactic Shock Shock resulting from widespread hypersensitivity. Form of distributive shock. Killer Bee .

 Drugs: ◦ Penicillin and related antibiotics ◦ Aspirin ◦ Trimethoprimsulfamethoxazole (Bactrim. Septra) ◦ Vancomycin ◦ NSAIDs  Other: ◦ Hymenoptera stings ◦ Insect parts and molds ◦ X-Ray contrast media (ionic)  Foods and Additives: ◦ Shellfish ◦ Soy beans ◦ Nuts ◦ Wheat ◦ Milk ◦ Eggs ◦ Monosodium glutamate ◦ Nitrates and nitrites ◦ Tartrazine dyes (food colors) Anaphylactic Shock .

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Septic Shock Component of systemic inflammatory response syndrome (SIRS). . Form of distributive shock.

Patient has nidus of infection. Causative organism releases: ◦ Endotoxin  Toxic shock syndrome toxin-1  Toxin A (Pseudomonas aeruginosa) ◦ Structure Components  Teichoic acid antigen  Endotoxin ◦ Activates immune system cascade Septic Shock .

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Etiology & Hemodynamic Changes in Shock Etiology of shock Example CVP CO SVR VO2 sat preload hypovolemic low low high low contractility cardiogenic high low high low afterload distributive .

Etiology & Hemodynamic Changes in Shock (Afterload) ETIOLOGY OF SHOCK EXAMPLE CVP CO SVR VO2 SAT AFTERLOAD DISTRIBUTIVE Hyperdynamic Septic Low/High High Low High Hypodynamic Septic Low/High Low High Low/High Neurogenic Low Low Low Low Anaphylactic Low Low Low Low .

Stages of Shock Compensated ◦ The body’s compensatory mechanisms are able to maintain some degree of tissue perfusion. . Irreversible ◦ Tissue and cellular damage is so massive that the organism dies even if perfusion is restored. Decompensated ◦ The body’s compensatory mechanisms fail to maintain tissue perfusion (blood pressure falls).

What is the first physiological factor in the development of shock? VO2 < MRO2 So. what are the first symptoms you would expect to find? ◦ ↑ respiratory rate ◦ ↑ heart rate Clinical Findings .

What is often the second physiological response to the development of shock? Peripheral vasoconstriction What symptoms would you expect to see? ◦ pale skin ◦ cool skin ◦ weakened peripheral pulses Clinical Findings .

what physiological effects are seen? End-organ perfusion falls What symptoms would you expect to see? ◦ altered mental status ◦ decreased urine output Clinical Findings .As shock progresses.

what signs and symptoms would you expect to see? ◦ ◦ ◦ ◦ ◦ tachycardia tachypnea pupillary dilation decreased capillary refill pale cool skin Clinical Findings .As compensatory mechanisms fully engage.

When compensatory mechanisms fail. what signs and symptoms would you expect to see? ◦ ◦ ◦ ◦ ◦ ◦ hypotension falling SpO2 bradycardia loss of consciousness dysrhythmias death Clinical Findings .

Treatment Manage the emergency Determine the underlying cause Definitive management or support .

cardiac transplant) Cardiogenic Shock . CABG.Treatment: ◦ ◦ ◦ ◦ ◦ ◦ ◦ ◦ Oxygen Monitors Nitrates (if possible) Morphine or fentanyl Pressor support (dopamine or dobutamine) If no pulmonary edema. consider small fluid boluses IABP Definitive therapy (fibrinolytic therapy. ventricular assist device. PTCA.

Treatment: ◦ ◦ ◦ ◦ ◦ ◦ ◦ Oxygen Supine position Monitors IV access Fluid replacement Pressor support (rarely needed) Correct underlying cause Hypovolemic Shock .

Fluid replacement: ◦ Hypovolemia:  Isotonic crystalloids  Colloids ◦ Hemorrhage:  Whole blood  Packed RBCs  HBOCs  Isotonic Crystalloids Hypovolemic Shock .

Caveat: ◦ If shock due to trauma. and bleeding cannot be controlled. ◦ If bleeding can be controlled. Hypovolemic Shock . give only enough small fluid boluses to maintain radial pulse (SBP≈ 80 mm Hg). control bleeding and administer enough fluid or blood to restore normal blood pressure.

Treatment: ◦ ◦ ◦ ◦ ◦ ABCDE Fluid resuscitation with crystalloid PA catheter helpful in preventing overhydration. Look for other causes of hypotension Consider vasopressor support with dopamine or dobutamine ◦ Transfer patient to regional spine center Neurogenic Shock .

Subcutaneously) ◦ IV Fluids (crystalloids) ◦ Antihistamines ◦ ◦ ◦ ◦  Benadryl  Zantac Steroids Beta agonists Aminophylline Pressor support (dopamine. Treatment: ◦ Airway (have low threshold for early intubation) ◦ Oxygenation and ventilation ◦ Epinephrine (IV. dobutamine or epinephrine) Anaphylactic Shock . IM.

Treatment: ◦ ◦ ◦ ◦ ◦ ◦ ◦ ◦ ◦ Airway and ventilatory management Oxygenation IV fluids (crystalloids) Pressor support (dopamine. norepinephrine) Empiric antibiotics Removal of source of infection NaHCO3? Steroids? Anti-endotoxin antibodies Septic Shock .