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