ABDOMINAL COMPARTMENT SYNDROME ( ACS ) DR. SHEHATA AHMED MBBS,MD,MRCS (ENGLAND) SENIOR GENERAL SURGEON
Jul 16, 2015
ABDOMINAL COMPARTMENT SYNDROME ( ACS )
DR. SHEHATA AHMED
MBBS,MD,MRCS (ENGLAND)
SENIOR GENERAL SURGEON
ACS OUTLNES
INTRODUCTION
DEFINITION
CAUSES
TYPES OF ACS
PATHOPHYSIOLOGY
CLINICAL PICTURES
DIAGNOSIS
TREATMENT
CONCLUSIONS
INTRODUCTION
COMPARTMENT SYNDROME CAN DEVELOP INNEARLY EVERY PART OF THE BODY THESE INCLUDES…..
1. INCREASED INTRACRANIAL PRESSURE FROM CLOSED HEAD INJURIES
2. RENAL FAILURES FROM SHOCK ASSOCIATED WITH A.TUBULAR NECROSIS
3. COMPARTMENT SYNDROME LOWER EXTREMITY USUALLY ASSOCIATED PRIMARILY WITH ISCHAEMIA FROM ARTERIAL CLOSURE EG. A.POPLITEAL ART.THROMBOSIS OR EMBOLISM,ILIAC ART. OCCLUSION&ILIOFEMORAL ART.INJ WITH SHOCK
INTRODUCTION ABDOMINAL COMPARTMENT SYNDROME (ACS)
OCCURS WHEN ABDOMEN BECOME SUBJECT TO INCREASED PRESSURE LEADING TO DECREASED BLOOD FLOW TO ABDOMINAL ORGANS AND IMPAIRS PULOMONARY,CVS,RENAL &GIT FUNCTION CAUSING MODS (MULTIPLE ORGAN DYSFUNCTION SYNDROME )&DEATH .
DEFINITION OF ACS
ADVERSE PHYSIOLOGICAL CONSEQUENCES THAT OCCUR AS A RESULT OF AN ACUTE INCREASE IN INTRAABDOMINAL PRESSURE(IAP)
INCREASED ABDOMINAL PRESSURE WITH INCREASED AIRWAY PRESSURE ,HYPOXIA&OLIGURIA
MULTIPLE ORGANS DYSFUNCTION CAUSED BY ELEVATED IAP
CAUSES OF ACS MAJOR ABD. INJURIES BLUNT OR PENETRATING
INTRAPERITONEAL OR RETROPERITONEAL HAEMORRHAGE SECONDARY TO TRAUMA OR RUPTURE AAA
MASSIVE FLUID RESUSCITATION
SEVERE SEPSIS
PANCREATITIS
ABD WALL BURN ESCHAR
LIVER DISEASE &LIVER TRANSPLANTATION
CAUSES
CLOSURE OF THE ABDOMEN UNDER UNDUE TENSION
ABDOMINAL PACKING FOR CONTROL OF HAEMORRHAGE DURING DAMAGE CONTROL SURGERY
PARALYTIC ILEUS & BOWEL OBSTRUCTION
TYPES OF ACS
PRIMARY ACS
INTRAABDOMINAL PATHOLOGY IS DIRECTLY
RESPONSIBLE FOR ACS EG……ABDOMINOPELVIC SURGERY…AFTER DAMAGE CONTROL SURGERY…PENETRATING ABDOMINAL INJURIES …PELVIC FRACTURE WITH BLEEDING…MASSIVE RETROPERITONEAL HAEMATOMA…LIVER TRANSPLANTATION
TYPES
SECONDARY ACS THIS OCCUR WHEN NO VISIBLE INTRAABDOMINAL PATHOLOGY IS THERE BUT THE CAUSE OUTSIDE THE ABDOMEN CAUSING FLUID ACCUMULATION EG….SEPSIS AND BURN
TERTIARY ACSACS RECURRING AFTER TREATMENT OF 1RY ACS
ANOTHER CALSSIFICATION
PRIMARY
SECONDARY
CHRONIC ACS LATE STAGES OF HEPATIC CIRRHOSIS &ASCITES
ACS
PATHOPHYSIOLOGY OF ACS
CENTRAL NERVOUS SYSTEM INCREASED INTRAABDOMINAL PRESSURE (IAP) WILL LEAD TO ….
INTRACRANIAL PRESSURE
CEREBRAL PERFUSION PRESSURE
PATHO.
CARDIOVASCULAR SYSTEM
IAP WILL CAUSE COMPRESSION OF AORTA &IVC CAUSING…VENOUS RETURN TO THE HEARTCARDIAC OUTPUTTISSUE PERFUSIONCVP&PAWP
SVR*CARDIAC INSUFFICENCY &CARDIAC ARREST
PATHO.
PULOMONARY INCREASED IAP WILL CAUSE DIAPHRAGMATIC COMRESSION CAUSING ……* INCREASAED INTRATHORACIC PRESSURE* INC.PAK INSPIRATORY PRESSURE* INC. AIRWAY PRESSURE* DECREASED COMPLIANCE * ATELECTASIS* DEC.PO2 (HYPOXIA ),HYPERCARBIA & ARDS* INC. INTRATHORA.PRE ALSO WILL LEAD TO DEC VENOUS RETURN EXACERBATING CARDIAC PROPLEM
PATH.
RENALINCREASED IAP CAUSES COMPRESSION OF THE RENAL ARTERIES &VEINS CAUSING…..* DECREASED RENAL BLOOD FLOW* DEC. GFR* DEC. URINE OUTPUT* A.TUBULAR NECROSIS* OLIGURIA,ANURIA & RENAL FAILURE
PATH.
GASTROINTESTINAL TRACTINCREASED IAP CAUSES COMPRESSION &CONGESTION OF THE MESENTERIC VEINS AND CAPILLARIES RESULTING IN…..
*DEC. SPLANCHNIC BLOOD FLOW*DEC. PH *DEC. GUT PERFUSION LEADING TO ISCHAEMIA ,NECROSIS ,CYTOKINE RELEASE ,BACTERIAL TRANSLOCATION & DEVELOPMENT OF SIRS FURTHER INCR. IAP
PATH.
ABDOMINAL WALLINCR. IAP CAUSING …..* DEC. COMPLIANCE* DEC. RECTUS SHEALTH BLOOD FLOW
MISCELLANEOUS
INCREASED IAP WILL CAUSE…..** DECREASED PERFUSION OF SURGICAL &TRAUMATIC WOUNDS LEADING TO POOR WOUND HEALING& DEHISCENCE** BLOOD POOLING IN PELVIS &LEGS WILL CAUSE DVT & PULMONARY EMBOLISM** DECREASED BLOOD FLOW TO LIVER AND BONE MARROW CAUSING COAGULOPATHY &IMMUNOSUPPRESION*** FINALY LEADING TO THE LETHAL TRIAD OF ACIDOSIS ,HYPOTHERMIA &COAGULOPATHY.
PHYSIOLOGIC INSULT
ISCHAEMIA INFLAMMATORY RESPONSE
CAPILLARY LEAK
FLUID RESUSCITATION
TISSUE OEDEMA
INCLUDING BOWEL WALL &MESENTRY
INTRAABDOMINAL HYPERTENSION(IAH)
Physiologic Insult/Critical Illness
Ischemia Inflammatory response
Capillary leak
Tissue Edema (Including bowel wall and mesentery)
Intra-abdominal hypertension
Fluid resuscitation
PATH.-DIAGRAM
SOFT TISSUE INJURY ISCHAEMIA
OEDEMA &INC. TISSUE PRESSURE
INCR.CELLULAR OEDEMA DEC.TISSUE PERFUSION
CRITICAL CAPILLARY
CELLULAR ISCHAEMIA CLOSING PRESSURE
TISSUE DEATH
PATHO.
APP = MAP - IAP
ABDOMINAL PERFUSION PRESSURE = MEAN ARTERIAL PRESSURE - INTRAABDOMINAL PRESSURE
APP REFLECT ACTUAL GUT PERFUSION BETTER THAN IAP ALONE
INCREASE IAP WILL LEAD TO DECREASED BLOOD FLOW TO THE ABDOMINAL VISCERA
APP WAS FOUND TO BE BETTER THAN OTHER RESUSCITATION ENDPOINTS EG. HOURLY URINE OUTPUT FOR PREDICTING THE OUTCOMES
APP
A TARGET OF APP OF AT LEAST 60 MMHG IS CORRELATED WITH IMPROVED SURVIVAL FROM IAH&ACS
IAH DEFINED AS SUSTAINED IAP AT OR MORE THAN 12 MMHG
ACS IS DEFINED AS SUSTAINED IAP MORE THAN 20 MMHG THAT IS ASSOCIATED WITH NEW ORGAN DYSFUNCTION
GRADES OF INTRAABDOMINAL
HYPERTENSION (IAH)NORMAL IAP 0-5 MMHG
GRADE 1 12-15 MMHG
GRADE 2 16-20 MMHG
GRADE 3 21-25 MMHG
GRADE 4 MORE THAN 25 MMHG
COMPLIANCE
COMPLIANCE = DELTA V/ DELTA P
V CHANGE IN VOLUME
P CHANGE IN PRESSURE
COMPARTMENT SYNDROME RESULT FROM INTRACOMPARTMENTAL HYPERTENSION THIS HYPERTENSION PRODUCE DYSFUNCTION WHICH IS INVERSELY PROPORTIONAL TO THE COMPLIANCE OF THE EFFECTED COMPARTMENT
Compliance
volume
Pressu
re
COMPLIANCE
THE APPROXIMATE PRESSURE OF 25 MMHG IS THE CRITICAL COMPARTMENT PRESSURE FOR SIGNIFICANT ALTERATION IN MICROVASCULAR BLOOD FLOW TO THE COMPARTMENTAL CONTENTS IN ESSENTIALLY ALL PARTS OF THE BODY
CLINICAL SIGNS & DIAGNOSIS OF ACS
TENSE ABDOMEN
INCREASED AIRWAY PRESSURE
DECREASED URINE OUTPUT
MONITORING OF INTRAABDOMINAL PRESSURE &ABDOMINAL PERFUSION PRESSURE
IAP MONITORING BLADDER PRESSURE MONITORING THROUGH THE
FOLEY CATHETER ( TRANSVESICAL ) IS THE CURRENT STANDARD FOR MONITORING ABD PRESSURE (INDIRECT GOLD STANDARD )
TRANRECTAL TRANSFEMORAL TRANSVAGINAL TRANSOESOPHOGEAL INTRAGASTRIC TRANSDUCER AS IN LAPAROSCOPY(GOLD
STANDARD IDEAL IS SIMULTANEOUS INTRAOESOPHOGEAL
&INTRAGASTRIC PRESSURE .
TREATMENT OF ACS
MEDICALCORRECT ELECTROLYTE BALANCEPROMOTE MOTILITYNEOSTIGMINERED. INTRAABDOMINAL FLUID &OEDEMA….
LASIX,ALBUMIN,LIMIT FLUID INTAKECT GUIDED ASPIRATION
PARACENTESISINC.ABD COMPLIANCE BY MUSCLE RELAXAT.,NEGATIVE PRESSUREDECOMPRESSION BY BOWEL BY ENEMA
( NOT EFFECTIVE ONLY BUY TIME FOR DEFINITIVE TREAT.)
MEDICAL TREATMENT
DECOMPRESSION COCKTAIL BEFORE DECOMPRESSIVE LAPAROTOMY….
IL NORMAL SALINE50 GM MANNITOL FOR DIUERESIS100 MMOL SODIUM BICARBONATE TO NEUTRALIZE ACIDOSIS
SURGICAL MANAGEMENT OF COMPARTMENT SYNDROMES
COMPARTMENT PATHOPHYSIOLOGY SURGICAL TREATMENT
CRANIUM INCREASED ICP MANNITOL/CRANIECTOMY
CHEST TENSION PNEUMOTHORAX
ICT(CHEST TUBE)
PERICARDIUM CARDIACTAMPONADE
PERICARDIOCENTESIS
LIMB EXTREMITY COMPARTMENTSYNDROME
FASCIOTOMY
ACS INCR. IAP&IAH DECOMPRESSIONLAPAROTOMY
DECOMPRESSIVE LAPAROTOMY
ACS
SURGICAL TREATMENT ACS
DECOMPRESSION LAPAROTOMY FOLLOWED BY …..
*** TEMPORARY CLOSURE TECHNIQUE(LAPAROSTOMIES)*** ON DEMAND RELAPARATOMY*** STAR (STAGED ABDOMINAL REPAIR)
TEMPORARY CLOSURE TECHNIQUE(LAPAROSTOMIES)
BOGOTA BAG CLOSURE -----A 3 L.PLASTIC IRRIGATION BAG IS EMPTIED & CUT OPEN SO IT LIES FLAT THE, EDGES ARE TRIMMED &SUTURED TO THE SKIN AWAY FROM THE SKIN EDGES
TOWEL CLIP CLOSURE (ABANDONED)
POLYPROPYLENE MESH
GRANULATED VICRYL/POLYGLYCOLIC ACID MESH
LAPAROSTMIES
VACUUM ASSISTED WOUND CLOSURE
( VACUUM PACK ) SPONGE IS PLACED TO PROECT THE GUT
2 SUCTION DRAINS PLACED OVER THIS LARGE ADHERENT STERIDRAPE PLACED OVER THE WHOLE ABDOMENAND SUCTION CATHETER CONNECTED TO A HIGH CONTINUOUS SUCTION EVACUATING THE ABDOMINAL CAVITY OF OEDEMA FLUID.
STAR ( ABDOMINAL WALL RECONSTRUCTION)
STAGED MANAGEMENT TECHNIQUE
STAGE 1 PROSTHETIC INSERTION 2-3WS
STAGE 2 PLANNED VENTRAL HERNIA THE
MESH REMOVED &SPLIT THICKNESS SKIN GRAFT USED TO CLOSE THE ABD.WALL ---(6-12 MONTHS)----
STAGE 3 DEFINITIVE RECONSTRUCTIONUSING * PROSTHETIC MATERIALS POLYPRO.MESH/PTFE
* APPLICATION OF MYOFASCIAL ADVANCEMENT TECHNIQUE,ROTATIONAL MUSCLE FLAP,…..
STAR
BIOMATERIALS RECENTLY USED ---HUMAN CADAVERIC ACELLULAR DERMIS FOR RECONSTRUCTION (ALLODERM)
COMPONENTS SEPARATION TECHNIQUE SIMPLY LOCAL MYOCUTANEOUS ADVANCEMENT FLAP AFTER EXTENSIVE RELAXING INCISION IN THE ABDOMINAL WALL INVOLVING BILATERAL MEDIAL MOBILISATION OF THE RECTUS ABDOMINUS MUSCLE (6-10 CM )
MODIFIED COMPONENT SEPARATION TECHNIQUE ---PROVIDE GOOD RESULTS (10-20 CM).
SUMMARY
ACS IS ACLINICAL ENTITY CAUSED BY PROGRESSIVE INCREASE IN IAP
MULTIPLE ORGAN SYSTEMS ARE EFFECTED USUALLY IN AGRADED FASHION THIS MEAN THAT ACS IS NOT JUST AN ABDOMINAL PROPLEM BUT RATHER A SYSTEMIC CONDITION
THE GUT IS THE ORGAN MOST SENSITIVE TO IAH
SUMMARY
SINCE THIS SYNDROME AFFECT PATIENTS WHO ARE ALREADY PHYSIOLOGICALLY COMPROMISED A HIGH DEGREE OF SUSPICION&LOW THRESHOLD FOR CHECKING IAP ARE REQUIRED TO PREVENT THE MORTALITY ASSOCIATED WITH THIS COMPLEX PROPLEM
MONITOR ALL HIGH RISK PAT. EARLY & DONOT WAIT FOR SIGNS OF ACS TO BE PRESENT BEFORE YOU DECIDE TO CHECK IAP
SUMMARY
FOCUS ON THE APP AS THE THERAPEUTIC ENDPOINT
TREATMENT INVOLVE DECOMPRESSION OF THE ABDOMEN
DELAY IN ABDOMINAL DECOMPRESSION MAY LEAD TO INTESTINAL ISCHAEMIA TO MOD SYNDROME AND DEATH SO DECOMPRESS EARLY
ACS IS A FIELD OF ONGOING RESEARCH.
THANK YOU