Interuniversitair Postgraduaat Onderwijs Heelkunde · delivery of killing forces to the area of...

Interuniversitair Postgraduaat Onderwijs Heelkunde

1° - 2° jaars ASO heelkunde

W-J. MetsemakersDienst Traumatologie

UZ Leuven

Postgraduaat Onderwijs: Traumatologie• Case Presentation

• Shock

• Trauma- Advanced Trauma Life Support (ATLS)- Definitive Surgical Trauma Care (DSTC)

• Surgical techniques- Fasciotomy- Diagnostic peritoneal lavage

Case presentation• Patient, 40 years

• Motor vehicle accident

• Vital signs:Sat: 88% (15l O2)P: 120/minBP: 100/60mmHg

• Rx cervical spine - pelvis – FAST: negative

Case presentation

Case presentation

Chest tube (left).

• Sat: 90% (15l O2)

• P: 100/min

• BP: 90/48mmHg

• ……?

Case presentation

Hemodynamicunstable!

Case presentation

‘’Shock is the manifestation of the rudeunhinging of the machinery of life’’Samuel V. Gross, 1872

Shock

http://en.wikipedia.org/wiki/File:Samuel_David_Gross_2.jpg

Modern definition:

Shock consists of inadequate tissue perfusion markedby decreased delivery of required metabolic substratesand inadequate removal of cellular waste products.

Shock

Classification of shock

• Hypovolemic

• Cardiogenic

• Septic (vasogenic)

• Neurogenic

• Traumatic

• Obstructive

Shock

Pathophysiology of shock• The initial insult, whether hemorrhage, injury, or infection, initiates both a

neuroendocrine and inflammatory mediator response.

• The physiologic responses to hypovolemia are directed at preservation of perfusion to the heart and brain: - vasoconstriction

- fluid excretion - fluid is shifted into the intravascular space.

• The major mechanisms achieving this response are: - prompt increase in cardiac contractility and peripheral

vascular tone via the - autonomic nervous system- hormonal response to preserve salt and intravascular

volume

Shock

Pathophysiology of shock• With substantial physiologic compensatory mechanisms for small volume

blood loss, predominantly through the neuroendocrine response, hemodynamics may be maintained compensated phase of shock.

• With continued hypoperfusion often not apparent clinically, cell death and tissue injury are ongoing decompensation phase of shock.

Shock

Hypovolemic shock• The most common cause of shock in the surgical or trauma patient is loss

of circulating volume from hemorrhage.

• Peripheral vasoconstriction is prominent, although lack of sympathetic effects on cerebral and coronary vessels and local autoregulation promote maintenance of cardiac and CNS blood flow.

Shock

Shock in a trauma patient and postoperative patient should be presumed to be because of hemorrhage until proven otherwise!

Cardiogenic shock• Cardiogenic shock is defined clinically as circulatory pump failure leading

to diminished forward flow and subsequent tissue hypoxia, in the setting of adequate intravascular volume

• Hemodynamic criteria - sustained hypotension (i.e., SBP

Cardiogenic shock• Most common cause : acute myocardial infarction (MI)

• Cardiogenic shock complicates 5–10 % of acute MIs

• The most common cause of death in patients hospitalized with acute MI

• Although shock may develop early after myocardial infarction, it is typically not found on admission

Shock

Cardiogenic shock: pathophysiology:• The pathophysiology of cardiogenic shock involves a vicious cycle of

myocardial ischemia which causes myocardial dysfunction, which results in more myocardial ischemia.

• When sufficient mass of the left ventricular wall is necrotic or ischemic and fails to pump, the stroke volume decreases.

• Decreased compliance results from myocardial ischemia, and compensatory increases in left ventricular filling pressures progressively occur.

Shock

ShockTable 1. Causes of Cardiogenic ShockAcute Myocardial Infarction

- Pump failureLarge InfarctionSmaller infarction with pre-existing diseaseRight Ventricular failure

- Mechanical complicationsPapillary muscle ruptureVentricular septal defectCardiac ruptureTamponade

Other CondtionsEnd-stage cardiomyopathyMyocarditisDrugs – eg beta-blocker overdoseAortic dissection with acute aortic regurgitationMyocardial contusionLeft ventricular outflow tract obstruction

Cardiogenic shock: diagnosis:• Confirmation of a cardiac source for the shock requires:

- electrocardiogram

- echocardiography

• Other useful diagnostic tests include chest radiograph, arterial blood gases, electrolytes, complete blood count, and cardiac enzymes.

Shock

Relatively few patients with blunt cardiac injury will develop cardiac pump dysfunction. Those who do generally exhibit cardiogenic shock early in their

evaluation.

Cardiogenic shock: treatment:• Intubation and mechanical ventilation are often required, if only to

decrease work of breathing and facilitate sedation of the patient.

• Treatment of cardiac dysfunction includes maintenance of adequate oxygenation to ensure adequate myocardial oxygen delivery and judicious fluid administration to avoid fluid overload and development of cardiogenic pulmonary edema.

• Cave electrolyte abnormalities and dysrrhythmias

• When profound cardiac dysfunction exists, inotropic support may be indicated to improve cardiac contractility and cardiac output:

- Dobutamine- Dopamine- (Cave Epinephrine)

Shock

Cardiogenic shock: treatment:

• Patients whose cardiac dysfunction is refractory to cardiotonics may require mechanical circulatory support with an intraaortic balloon pump (IABP). Intraaortic balloon pumping increases cardiac output and improves coronary blood flow by reduction of systolic afterload and augmentation of diastolic perfusion pressure

• Anticoagulation and aspirin are given for acute myocardial infarction

• Additional pharmacologic tools may include the use of: β blockers, nitrates and ACE inhibitors

Shock

Cardiogenic shock: treatment:• Current guidelines of the American Heart Association (AHA): percutaneous

transluminal coronary angiography (PTCA) for patients with:- cardiogenic shock- ST elevation (left bundle-branch block)- age younger than 75 years

• Early definition of coronary anatomy and revascularization is the pivotal step in treatment of patients with cardiogenic shock from acute MI. When feasible, PTCA (generally with stent placement) is the treatment of choice

• Coronary artery bypass grafting (CABG) seems to be more appropriate for patients with multiple vessel disease or left main coronary artery disease

Shock

Septic (vasogenic) shockIn vasodilatory shock, hypotension results from failure of the vascular smooth muscle to constrict appropriately.

Vasodilatory shock is characterized by both peripheral vasodilatation with resultant hypotension, and resistance to treatment with vasopressors.

The most frequently encountered form of vasodilatory shock is septic shock.

Other causes of vasodilatory shock include: - hypoxic lactic acidosis- carbon monoxide poisoning- decompensated and irreversible hemorrhagic shock- terminal cardiogenic shock- postcardiotomy shock

Shock

Septic (vasogenic) shock• In the attempt to eradicate the pathogens, the immune and other cell types

elaborate soluble mediators that enhance macrophage and neutrophil killing effector mechanisms, increase procoagulant activity and fibroblast activity to localize the invaders, and increase microvascular blood flow to enhance delivery of killing forces to the area of invasion

• These findings include enhanced cardiac output, peripheral vasodilation, fever, leukocytosis, hyperglycemia, and tachycardia nitric oxide (NO)

Shock

Septic (vasogenic) shock: diagnosis:• Patients with sepsis have evidence of an infection and systemic signs of

inflammation (e.g., fever, leukocytosis, and tachycardia).

• Recognizing septic shock begins with defining the patient at risk.

• The clinical manifestations of septic shock will usually become evident and prompt the initiation of treatment before bacteriologic confirmation of an organism or the source of an organism is identified.

• These should prompt an aggressive search for infection including:- thorough physical exam- inspection of all wounds- evaluation of intravascular catheters or other foreign bodies- obtaining appropriate cultures and adjunctive imaging studies as needed

Shock

Septic (vasogenic) shock: treatment:• Evaluation of the patient in septic shock begins with an assessment of their

airway and ventilation Intubation

• Because vasodilation and decrease in total peripheral resistance may produce hypotension, fluid resuscitation is essential

• Empiric antibiotics must be chosen carefully based on the most likely pathogens. Antibiotics should be tailored to cover the responsible organisms once culture data are available

• Intravenous antibiotics will be insufficient to treat the infection in the settings of infected collections, foreign bodies, and devitalized tissue Surgery

• After first-line therapy vasopressors may be necessary to treat patients with septic shock

Shock

Neurogenic shock• Neurogenic shock refers to diminished tissue perfusion as a result of loss

of vasomotor tone to peripheral arterial beds.

• Sympathetic input to the heart and input to the adrenal medulla may also be disrupted preventing the typical reflex tachycardia that occurs with hypovolemia.

• Neurogenic shock is usually secondary to spinal cord injuries from vertebral body fractures of the cervical or high thoracic region that disrupt sympathetic regulation of peripheral vascular tone.

Shock

Neurogenic shock: diagnosis:• Acute spinal cord injury may result in bradycardia, hypotension, cardiac

dysrhythmias, reduced cardiac output, and decreased peripheral vascular resistance.

• The classic description of neurogenic shock consists of:

- decreased blood pressure associated with bradycardia

- warm extremities

- motor and sensory deficits indicative of a spinal cord injury

- radiographic evidence of a vertebral column fracture

Shock

In the multiply injured patient, other causes of hypotension including hemorrhage, tension pneumothorax, and cardiogenic shock must be

sought and excluded!!!

Neurogenic shock: treatment:• After the airway is secured and ventilation is adequate, fluid resuscitation

and restoration of intravascular volume will often improve perfusion in neurogenic shock.

• Administration of vasoconstrictors will improve peripheral vascular tone, decrease vascular capacitance, and increase venous return.

• Specific treatment for the hypotension is often of brief duration, as the need to administer vasoconstrictors typically lasts 24–48 hours.

Shock

First exclude hypovolemia as the cause of the hypotension.

Traumatic shock• The systemic response after trauma, combining the effects of soft-tissue

injury, long-bone fractures, and blood loss, is clearly a different physiologic insult than simple hemorrhagic shock.

• The hypoperfusion deficit in traumatic shock is magnified by the proinflammatory activation that occurs following the induction of shock.

• Treatment of traumatic shock is focused on correction of the individual elements to diminish the cascade of proinflammatory activation, and includes prompt control of hemorrhage, adequate volumeresuscitation to correct oxygen debt, débridement of nonviable tissue, stabilization of bony injuries, and appropriate treatment of soft tissue injuries.

Shock

Obstructive shock• Commonly mechanical obstruction of venous return in trauma patients is

because of the presence of tension pneumothorax and cardiac tamponade.

• With either cardiac tamponade or tension pneumothorax, reduced filling of the right side of the heart from either increased intrapleural pressure secondary to air accumulation or increased intrapericardial pressure results in decreased cardiac output associated with increased central venous pressure.

Shock

Obstructive shock• The diagnosis of tension pneumothorax should be made on clinical

examination.

• The classic findings include:

- respiratory distress

- hypotension

- diminished breath sounds over one hemithorax

- hyperresonance to percussion

- jugular venous distention

- shift of mediastinal structures

Shock

Treatment with pleural decompression is indicated rather than delaying to wait for radiographic confirmation.

Obstructive shockCardiac tamponade results from the accumulation of blood within the pericardial sac, usually from penetrating trauma or chronic medical conditions.

Triad of Beck consists of hypotension, muffled heart tones, and neck vein distention.

Patients who present with circulatory arrest from cardiac tamponade require emergency pericardial decompression, usually through a left thoracotomy.

Echocardiography has become the preferred test for the diagnosis of cardiac tamponade.

Shock

Obstructive shockPericardiocentesis to diagnose pericardial blood and potentially relieve tamponade may be used. An in-dwelling catheter may be placed for several days in patients with chronic pericardial effusions.

Diagnostic pericardial window represents in chronic cases the most direct method to determine the presence of blood within the pericardium. The procedure is best performed in the operating room under general anesthesia.

Shock

• The Advanced Trauma Life Support (ATLS) course of the American College of Surgeons Committee on Trauma was developed in the late 1970s, based on the assumption that appropriate and timely care can significantly improve the outcome for the injured patient.

• ATLS provides a structured approach to the trauma patient with standard algorithms of care; it emphasizes the "golden hour" concept that timely prioritized interventions are necessary to prevent death.

Trauma: introduction

• The initial management of seriously injured patients consists of the primary survey, concurrent resuscitation, the secondary survey, diagnostic evaluation, and definitive care.

• The first step in patient management is performing the primary survey, the goal of which is to identify and treat conditions that constitute an immediate threat to life.


• The ATLS course refers to the primary survey as assessment of the "ABCs" (Airway with cervical spine protection, Breathing, and Circulation).

• Although the concepts within the primary survey are presented in a sequential fashion, in reality they often proceed simultaneously.


Life-threatening injuries must be identified and treated before advancing to the secondary survey.

• Assess a patient’s condition rapidly and accurately.

• Resuscitate and stabilize patients according to priority.

• Determine whether a patient’s needs exceed a facility’s resources and/or a doctor’s capabilities.

• Arrange appropriately for a patient’s interhospital or intrahospital transfer (what, who, when, and how).

• Ensure that optimal care is provided and that the level of care does not deteriorate at any point during the evaluation, resuscitation, or transfer processes.


• Airway maintenance with cervical spine protection assessment of a free airway so oxygen can be transported

• Breathing and ventilation Without adequate air intake there is no oxygen for transport

• Circulation with hemorrhage control Circulating volume and heart need to be intact to transport oxygen to the brain and the tissues

• Disability: Neurologic status Check the neurological status of the patient

• Exposure/ Environment control: Completely undress the patient, but prevent hypothermia Keep the patient warm and save


Treat first what kills first!

Trauma: introductionTable 7-1 Immediately Life-Threatening Injuries to Be Identified during the

Primary Survey

Airway

Airway obstruction

Airway injury

Breathing

Tension pneumothorax

Open pneumothorax

Flail chest with underlying pulmonary contusion

Circulation

Hemorrhagic shock

Massive hemothorax

Massive hemoperitoneum

Mechanically unstable pelvis fracture

Extremity losses

Cardiogenic shock

Cardiac tamponade

Neurogenic shock

Cervical spine injury

Disability

Intracranial hemorrhage/mass lesion

‘Blood on the floor….plus four more (chest, abdomen, pelvis, femur)’

AIRWAY MANAGEMENT WITH CERVICAL SPINE PROTECTION• Ensuring a patent airway is the first priority in the primary survey.

• Simultaneously, all patients with blunt trauma require cervical spine immobilization until injury is excluded.

• In general, patients who are conscious, do not show tachypnea, and have a normal voice do not require early attention to the airway.

• In the comatose patient, the tongue may fall backward and obstruct the hypopharynx; this may be relieved by either a chin lift or jaw thrust.


AIRWAY MANAGEMENT WITH CERVICAL SPINE PROTECTION• Options for endotracheal intubation include: - nasotracheal route

- orotracheal route

- surgical routes

• Orotracheal intubation is the most common technique used to establish a definitive airway

• Because all patients are presumed to have cervical spine injuries, manual in-line cervical immobilization is essential

• Patients in whom attempts at intubation have failed or who are precluded from intubation due to extensive facial injuries require surgical establishment of an airway Cricothyroidotomy


BREATHING AND VENTILATION• Once a secure airway is obtained, adequate oxygenation and ventilation

must be assured

• All injured patients should receive supplemental oxygen and be monitored by pulse oximetry

• The following conditions constitute an immediate threat to life due to inadequate ventilation and should be recognized during the primary survey: - tension pneumothorax

- open pneumothorax

- flail chest with underlying pulmonary contusion


CIRCULATION WITH HEMORRHAGE CONTROL• An initial approximation of the patient's cardiovascular status can be

obtained by palpating peripheral pulses.

• In general, systolic blood pressure (SBP) must be:

- 60 mmHg for the carotid pulse to be palpable

- 70 mmHg for the femoral pulse to be palpable

- 80 mmHg for the radial pulse to be palpable


Any episode of hypotension (defined as a SBP

CIRCULATION WITH HEMORRHAGE CONTROL• IV access for fluid resuscitation is obtained with two peripheral catheters,

16-gauge or larger in adults

• Blood should be drawn simultaneously and sent for measurement of hematocrit level, as well as for typing and cross-matching

• If peripheral access with large-bore angiocatheters is inadequate different options are possible: - central venous line

- saphenous vein cutdowns

- intraosseous needle


CIRCULATION WITH HEMORRHAGE CONTROL• Cause of bleeding: ‘blood on the floor + 4 more (chest, abdomen, pelvis

femur)’

• Diagnostics: Chest x-ray, x-ray of the pelvis and FAST


Shock in the trauma patient is most commonly due to Hemorrhage.

Treatment of hemorrhagic Shock:• First check if A and B are stable

• Check the initial response and act according to the response.

-Rapid response

-Transient response

-Minimal or no response


Stop the bleeding!!!

Treatment of hemorrhagic Shock:• Fluid resuscitation begins with a 2 L (adult) or 20 mL/kg (child) IV bolus of

isotonic crystalloid, typically Ringer's lactate.

• For persistent hypotension, this is repeated once in an adult and twice in a child before red blood cells (RBCs) are administered.

• The Urine output is a quantitative, reliable indicator of organ perfusion. Adequate urine output is 0.5 mL/kg per hour in an adult, 1 mL/kg per hour in a child, and 2 mL/kg per hour in an infant

DISABILITY AND EXPOSURE• The Glasgow Coma Scale (GCS) score should be determined for all injured

patients

• It is calculated by adding the scores of the best motor response, best verbal response, and eye opening

• Scores range from 3 (the lowest) to 15 (normal)

• Scores of: - 13 to 15 indicate mild head injury

- 9 to 12 indicate moderate head injury

-

DISABILITY AND EXPOSURE• Establish the patient's: - level of consciousness

- pupil size and reaction

- lateralizing signs


Neurologic evaluation before administration of neuromuscular blockade for intubation is critical!

• in 85% of all trauma

• often appear dramatic, rarely cause immediate threat to life or limb

• correct assessment prevent later mortality-morbidity

• injury ~ energy

• 1st ABCDE

• Primary and secondary survey

• continuous re-evaluation!

Musculoskeletal trauma

Definitive Surgical Trauma Care

Case presentation

‘MIST’ Handover

• M: Mechanism

• I: Injuries sustained

• S: Signs on scene

• T: Treatment

Case presentation

Male patient, age: 48 years

• Time of injury 09h00

• M:Gunshot

• I: Left upper quadrant of abdomen

• S: RR 38/min P 100/m BP 120/80 GCS 14/15

• T: 2.5 litres iv crystalloid

Case presentation

Primary Survey

• Arrival at 09h30 (30 minutes later)

• A: Patient talking

• B: Air entry decreased on left. RR 38/m

• C: P 120/m BP 90/60. Pale

• D: Alert GCS 15/15

Case presentation

• No external bleeding

• No exit wound

• Omentum protruding from abdominal wall

Chest tube? Further investigation? Transfer to OR

Case presentation

Case presentation

Left chest tube –minimal drainage

Transfer to O.R. 10h30

Urgent laparotomy

Senior help available

•Chief of Surgery

•Chief of Anaesthesiology

Case presentation

Operative findings• Distal stomach “doubtful viability”

• Transection of transverse colon

• Multiple small bowel perforations (6)

• Mesenteric lacerations

• Lacerations of left lobe of liver

Case presentation

Haemodynamically“stable”

•P 110/m BP 110/60 T 32.8 C

Gases –“reasonable”

•O2 saturation 94%

•pH 7.23

•Lactate 6

Oozing; not actively bleeding

• 8 units PRBC transfused

Case presentation

• Distal gastrectomy

• Multiple small bowel resections

• Liver lacerations repaired

• Resection of transverse colon

• Colostomy

• Operating time: 150 min

Patient becomes suddenly hypotensive!

Case presentation

Trans-diaphragmatic pericardial assessment

•Pericardial window. No tamponade

Transferred to ICU at 15h00

Fluids given in the ICU

•Colloid 3.5 litres

•Crystalloid 5 litres

•32 units blood

•12 Fresh frozen plasma (FFP)

•10 units platelets

Case presentation

Bleeding from colostomy

Liver CT scan – no active bleeding

Diffuse intravascular coagulopathy (DIC)

Died 2 days later: multi-organ failure!

Case presentation

Despite good „surgical technique‟, patient diedWhy?.......

•Failure in decision making

•Failure to know when to stop (gastrectomy, colon

resection, etc)

Appreciate the physiology! Damage control!

Damage Control Surgery

Definition

DCL is an abbreviated resuscitative surgical

approach with the primary goal being the rapid

control of hemorrhage and contamination focused

on restoring normal physiology.

Rotondo MF, et al. ‘Damage control’: an approach for improved survival in

Exsanguinating penetrating abdominal injury. J Trauma. 1993;35:375–382.

Five stages

Stage I: Patient selectionCritical factors (The deadly triad)• Hypothermia : Tº < 35°C• Severe metabolic acidosispH < 7.2 Lactate > 5 mmol/l

• Coagulopathy (INR or PTT >50% of normal)Massive transfusion

Secondary factors• Severe injury• Operating time > 90 minutes

Stage I: Patient selection

Stage II: DCS: Thoracic Trauma85% of patients do not require operation (chest Tube)

15% require operation

Stage II: DCS: Thoracic TraumaIndications Emergency Room Thoracotomy (ERT)

Penetrating injury patient ‘in extremis’:

• Witnessed cardiac arrest with electrical activity

• Hypotension (SBP < 60 mm Hg) not responding to adequate fluid Resuscitation

Stage II: DCS: Thoracic Trauma

Survival

Stage II: DCS: Thoracic TraumaERT: technique:Usually through the left chest (anterolateral)

Patient supine, slight rotation

Arm elevated if possible

5th intercostal space (under breast)

Cut down onto rib

Enter chest over the top of the rib

Stage II: DCS: Thoracic TraumaPericardial Tamponade:

Open pericardium in a cranio-caudal direction

Pitfall: damage to phrenic nerve

Stage II: DCS: Thoracic TraumaControl of the thoracic aorta:Retract left lung anteriorly

Slide hand around posterior chest wall – lateral to medial along ribs

First tubular structure against tip of fingers is the aorta

Divide overlying pleura transversely

Compress aorta against vertebra or clamp with a vascular clamp

Pitfall:

Confusing aorta and oesophagus


Further exploration and closure of the chest in the OR!!!

Stage II: DCS: Abdominal Trauma

Stage II: DCS: Laparotomy

•Scoop out as much blood as possible (Kidney dish (receiver))

•Eviscerate small bowel

•Rapid exploration for massive bleeding

•Pack abdomen as appropriate

Stage II: DCS: Laparotomy

Stage II: Haemorrhage control

Bleeding vessels/organs

•Ligate

•Shunt

•Repair

The blood loss is usually underestimated!!!

Stage II: Haemorrhage control

Liver Trauma

Generous laparotomy

Be prepared to extend

•Sternotomy

•Laterally -subcostal

Efficient retraction

(Omnitract®, etc.)

Liver Trauma

FIRST STEP: PUSH (manual compression and rapidcontrol)

Now stop and plan approach!

Liver Trauma

•Inspect without mobilization

•Compress manually - pack with large packs

•Check for and control other sites of bleeding

•Allow anaesthesiologist to catch up

•Wait at least 10 min

•If no further bleeding

•Remove packs

Liver TraumaMobilize liver if necessaryAdequate packs (as few as needed for haemostasis)

•Subdiaphragmatic•Subhepatically•Posterior to injured lobe•Beneath ribs or abdominal wall

Restore liver contoursLess effective for left lobePlastic lining of packs unnecessary

Liver Trauma

Perihepatic packing

Liver Trauma

No treatment required if bleeding has stopped and patient normotensive

Don‟t probe “soft spots”

If still bleeding Pringle Maneuver

Liver Trauma

Liver Trauma

Definitive Packing Indications:

• Developing intraoperative coagulopathy

• Failure to control haemorrhage

• Expanding subcapsular haematoma

• Damage control surgery

• Patient requires transfer

• Retrohepatic caval or other venous injury

Liver TraumaPack first

•Initial packing

Persistent bleeding•Pringle & direct vision

Remember damage control option•Definitive packing

Consider angiography & embolization

Resection rarely desirable or necessary

Splenic TraumaNonoperative treatment: growing in popularity (children > 90%)

Success NOT predictable by:•Grade of injury•Size of haemoperitoneum on CT

Risk of failure increases with:•Haemodynamic instability•Vascular blush on contrast CT•Age greater than 55 years

Splenic Trauma

Operative Management

Packing

Topical haemostasis

•Tachosil®

•Fibrin glue

Argon beam

Partial resection

Mesh

Splenectomy

Bloodless surgery of the spleen possible with warm ischaemia for 1 hour

Splenic Trauma

Generous access

• Left hand placed on spleen

Full mobilization

•Divide lienocolic lig.

•Divide lienorenal lig.

•Divide lienophrenic lig.

Splenic Trauma

Mobilize spleen medially

Individual ligation of

•Main vessels

•Vasa brevia

Beware tail of pancreas

Splenic TraumaBleeding

•From ligated splenic vessels (slipped ligature)

Gastric fistula•Gastric wall necrosis from ischaemia or clamp

Pancreatic fistula•Injury of tail of pancreas

Colonic fistula•Colonic damage during division of lienocolic lig

Diaphragmatic injury (missed)•Close proximity injury

Splenic Trauma

Preservation of the spleen is possible…..but not in adverse circumstances!Think Damage Control Surgery.

Pelvic Trauma• Mortality rate of haemodynamically unstable pelvic fractures: 40 –

60 %.

• Anatomical studies have discovered that the veins and the surfaces of the fractures are the major sources of haemorrhage in patients with severe pelvic fractures

5-10 % arterial bleeding!

Pelvic stabilisation: tamponade

Pelvic Trauma

Treatment • Endorotation legs (open book)

• Pelvic Binder:

The use of the pelvic stabilizer (T-POD) results in a reduced symphyseal diastasis of 60% and a

postive circulatory respons in 80% of the patients (E. Tan, S. Van Stigt, A. Van Vugt.: Injury: 2010).

• Operative management: (- C-clamp)

- External fixation

- Pelvic Packing

(- Definitive fixation)

Controversy about kind and timing of fixation.

Pelvic Trauma

Preperitoneal Pelvic Packing:• Vertical suprapubic incision

• Approach according to Stoppa

• Dissect as far posteriorly as possible

• Pack from below SI joint outwards

• Close fascia and skin

• Use external fixation or simple anterior ORIF to close and fix the ring

Pelvic Trauma

Angiographic Embolisation:Angiographic embolization (AE):

- First article published by Margolies 1972 (N Engl J Med).

- Efficacy of AE in controling pelvic arterial hemorrhage: > 90%.

Left inferior vesical artery

Pelvic Trauma

Treatment

REBOA

Primary Survey: control hemorrhage:– Deep soft tissue lacerations near major vessels:

PRESSURE

– Long bone fractures (eg femoral: 4U blood loss class III shock)

SPLINTING

- traction-alignement (NOT joints)

- ↓ pain,↓ motion, ° muscle tamponade, prevent further

soft tissue injury

- open fractures: + sterile pressure bandage


Aggressive fluid rescusitation!!!

Secondary survey: 3 goals:

– Identification of life threatening injury (primary)

– Identification of limb threatening injury (secondary)

– Systematic review to avoid missing diagnosis

(continuous re-eveluation)


Undressed (hypothermia)!!!

Musculoskeletal Trauma

Save Life Before Limb!!!

Stage II: Contamination control

Drainage

•No stomas

•Drains where appropriate

Closure

•Staples

•Tape

•Suture

Thorough washout with normal saline!!!

Stage II: Temporary closure

• “Opsite Sandwich” (“Vacpac”)

• VAC-system (ABThera)

• Tissue closure

Don’t suture sheath until definitive closure!!!


+ -


KCI-ABThera

Stage III: Restoration of physiology

Objectives:

•Core Temperature > 35°C

•Lactate

Stage IV: Return to the OR

When to transfer from ICU to OR?

•Prompt transfer is cost-effective

•Premature departure is not!

Ideally within 24 –72 hours!!!

Not too early!(patient/surgeon)

Not too late! (infection)

ConclusionRecognize those at risk early•Proper damage control early•Abort operation early!

Resuscitate in the I.C.U. early

Angiography with embolization

Work with other disciplines as team

Complete the planned surgery later

Surgical Techniques

• Fasciotomy of the lower leg

• Diagnostic peritoneal lavage

Compartment syndrome (CS): diagnosis:

• Pain out of proportion to the apparent injury (passive

stretch of the affected muscles).

• Pressure measurements alone are not reliable to rule out

the diagnosis: 1.) DBP-CP= ‘Delta-P’, 30 mmHg or less

suggests CS

2.) CP higher than 30 mmHg also suggests CS

Surgical Techniques: fasciotomy

Clinical Diagnosis!!!

Surgical Techniques: Fasciotomy

http://www.youtube.com/watch?feature=player_detailpage&v=6c5r5brMOso

Surgical Techniques: Fasciotomy

Fasciotomy: closure:

De huid niet primair sluiten!!!

• Diagnostic peritoneal lavage (DPL) is a highly accurate test for evaluating intraperitoneal hemorrhage or a ruptured hollow viscus.

• It is less frequently today due to the increased use of focused abdominal sonography for trauma (FAST) and helical computed tomography (CT).

Surgical Techniques: DPL


Aspirate 10ml of ‘gross blood or enteric contents’: positive DPL.


Criteria for "Positive" Finding on Diagnostic Peritoneal Lavage

• Red blood cell count > 100,000/mL

• White blood cell count > 500/mL

• Amylase level > 19 IU/L

• Alkaline phosphatase level > 2 IU/L

• Bilirubin level > 0.01 mg/dL

or

• Gramstain positive for bacteria

• De vragen van het examen komen uit de slides en de les

• De 2 video’s kunnen via de video-URL onderaan de site terug gevonden worden op youtube

• Denk bij ATLS voornamelijk aan de hoofdpunten: ABCD en in die volgorde!

• Veel succes

Exameninformatie

Interuniversitair Postgraduaat Onderwijs Heelkunde · delivery of killing forces to the area of...

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