Introduction
An important cause of AKI in a critical care setting.
Intra-abdominal pressure (IAP) is the pressure enclosed within the abdomen and usually correlates with BMI. Intra-abdominal hypertension (IAH) is defi ned as a persistent IAP of ≥ 12mmHg (with various grades of severity as IAP rises).
Increased IAP l d blood fl ow to abdominal viscera l organ dysfunction.
It strongly predicts adverse outcomes in critically ill patients.
Abdominal compartment syndrome (ACS) describes the syndrome of organ (including renal) dysfunction s to IAH. It is most often seen in an HDU/ICU setting where it may be diffi cult to diagnose amongst the com-plications of a primary disease.
Causes
• p ACS: disease/injury within the abdomen (e.g. trauma, surgery, ascites, bowel distension, intraperitoneal bleeding, liver transplantation, retroperitoneal disease — including AAA, pancreatitis).
• s ACS: disease/injury outside the abdomen (e.g. sepsis, burns, aggressive fl uid resuscitation).
Estimates of prevalence vary widely, e.g. 1 – 15% in the context of traumatic injury.
Consequences
• ACS can affect virtually organ system:
• CV: d venous return l reduced cardiac output.
• Respiratory: d chest compliance l respiratory compromise and i infection.
• GI: d mesenteric blood fl ow l bowel ischaemia. Venous congestion l gut oedema. Bacterial translocation l sepsis.
• Liver dysfunction l lactic acidosis.
Renal
• Renal vein compression l venous congestion.
• d cardiac output l SNS and RAS activation l renal vasoconstriction.
• Both of these l d RBF l glomerular perfusion l oliguria l AKI.
Clinical presentation
Abdominal pain, tenderness, bloating and distension, breathlessness (or i ventilatory requirements), i pulse, d BP, i JVP, d UO, peripheral oedema, lactic acidosis.
Diagnosis
Diagnosis requires recognition of at-risk patients and situations with appropriate measurement of the IAP.
ABDOMINAL COMPARTMENT SYNDROME (ACS) 163
IAP can be measured indirectly, using intra-gastric, intra-colonic, IVC, or intra-vesical (most common) catheters. The World Society of the Abdominal Compartment Syndrome recommends the latter (see Fig. 2.15). Commercial devices are available, although a pressure trans-ducer connected to a standard Foley catheter is often used.
Imaging is non-diagnostic.
Management
• Supportive care 9 surgical decompression:
• Supportive care: adequate analgesia, sedation, and muscle paralysis (with ventilatory support); consider NG and rectal decompression;
accurate fl uid management; nurse in supine position.
• Surgical decompression: early intervention as IAP rises (and prior to development of ACS) is increasingly advocated. The most common technique is midline decompression, leaving an open abdomen.
• Patients should be screened for IAH/ACS risk factors upon ICU admission and with new or progressive organ failure.
• If two or more risk factors are present, a baseline IAP measurement should be obtained
• If IAH is present, serial IAP measurements should be performed throughout the patient’s critical illness.
Patients has TWO or more risk factors for IAH/ACS upon either ICU admission
or in the presence of new or progressive organ failure
Risk factors for IAH/ACS 1. Diminished abdominal wall compliance • Acute respiratory failure, especially with elevated intrathoracic pressure • Abdominal surgery with primary fascial or tight closure
• Major trauma/burns
• Prone positioning, head of bed >30 degrees • High body mass index (BMI), central obesity
2. Increased intra-luminal contents • Gastroparesis • Ileus
• Colonic pseudo-obstruction
3. Increased abdominal contents • Haemoperitoneum/pneumoperitoneum • Ascites/liver dysfunction
4. Capillary leak/fluid resuscitation • Acidosis (pH <7.2) • Hypotension
• Hypothermia (core temperature <33°C) • Polytransfusion (>10 units of blood/24 hours) • Coagulopathy (platelets <55,000/mm3 OR Prothrombin time (PT) >15 seconds OR partial thromboplastin time (PTT) >2 times normal OR international standardised ratio (INR) >1.5) • Massive fluid resuscitation (>5L/24 hours) • Pancreatitis
• Oliguria • Sepsis • Major trauma/burns • Damage control laparotomy Sustained IAP ≥
12mmHg?
YES NO
Patients has IAH Patient does not
have IAH
IAH - intra-abdominal hypertension ACS - abdominal compartment cyndrome IAP - intra-abdominal pressure.
Abbreviations Grade I Grade II Grade III Grade IV
IAH grading IAP 12–15mmHg IAP 16–20mmHg IAP 21–25mmHg IAP ≥25mmHg Observe patient.
Recheck IAP if patient deteriorates clinically.
Notify patient’s doctor of elevated IAP.
Proceed to IAH/ACS management algorithm.
Measure patient’s IAP to establish baseline pressure IAP measurement should be:
1. Expressed in mmHg (1mmHg = 1.36cmH O) 2. Measured at end-expiration 3. Performed in the supine position 4. Zeroed at the iliac crest in the mid-axillary line 5. Performed with an instillation volume of no greater than 25mL of saline (1mL/kg for children up to 20kg) (for bladder technique)
6. Measured 30–60 seconds after instillation to allow for bladder detrusor muscle relaxation (for bladder technique)
7. Measured in the absence of active abdominal muscle contractions
Fig. 2.15 IAH assessment algorithm. Used with the kind permission of the World Society of the Abdominal Compartment Syndrome. M http://www.wsacs.org
AKI in the developing world
Introduction
The aetiology (and 6 presentation) of AKI may be different from that seen in developed countries, particularly in more rural areas. This may vary down to a regional level, depending on socio-economic and environmental factors.
However, basic pathophysiological and management principles still apply.
Epidemiology
Cases are underreported, so accurate epidemiological data are scarce.
However, community-acquired AKI is more common (estimate 7 150 pmp) and affects a younger age group (mean age 37 in one study from south-ern India). Mortality rates are also higher and more dependent on local resources. There may be less access to RRT in some areas, with peritoneal dialysis more commonly employed for this purpose ( b p. 188).
Overall, ‘medical ’ causes of AKI, such as sepsis, predominate; how-ever, cases related to surgery are rising, as increasing numbers of pro-cedures are undertaken in older, more comorbid patients. Fortunately, obstetric-associated AKI is in fairly rapid decline in most areas.
Causes
Infective causes of AKI
• Diarrhoeal disease:
• Common cause of pre-renal AKI and ATN (and HUS — see further in list).
• Children with diarrhoea are much more susceptible to AKI (diarrhoea causes 7 50% of dialysis-requiring AKI in Indian children).
• Viral causes: rotavirus and Norwalk agent.
• Bacterial causes: E. coli , Shigella spp., Salmonella enteritides, Vibrio cholera , Campylobacter jejuni , Pseudomonas aeruginosa , Klebsiella pneumoniae.
• Treatment is supportive ( l directed at fl uid and electrolyte imbalances) 9 antimicrobials for specifi c infections.
• Diarrhoea-associated (D+) haemolytic uraemic syndrome ( b p. 578) is common in paediatric practice internationally. It is most commonly associated with Shigella dysenteriae serotype 1 but has many other precipitants.
• Malaria ( b p. 702).
• Leptospirosis:
• Leptospira interrogans is a spirochaete that infects many mammalian species and is shed in urine.
• Illness classically follows a biphasic course, with an initial febrile illness, followed by more fulminant disease with liver involvement.
• AKI occurs in 7 50% of severe cases.
• Associated AKI may be pre-renal/ATN, but an interstitial nephritis (with marked urinary K + wasting) is also common.
• Diagnose with serology (late) or antigen detection via PCR (early).
• Treatment is supportive, plus penicillin, doxycycline, or 3rd-generation cephalosporin (e.g. ceftriaxone).
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• HIV ( b p. 676):
• AKI usually s to HIV-associated infection or HAART-related nephrotoxicity, but many other renal lesions are recognized.
• Melioidosis:
• Organism: Burkholderia pseudomallei . • Area: South East Asia and Northern Australia.
• Illness: pneumonia, visceral and cutaneous micro-abscesses, septicaemia.
• AKI in >50%. Renal micro-abscesses are common.
• Viral haemorrhagic fevers:
• Severe multisystem illnesses (including Dengue, Yellow, Ebola, Marburg, and Lassa fever) caused by 12 RNA viruses from four families (fl avi-, arena-, bunya-, and fi lovirus).
• Haemodynamic instability and increased vascular permeability l ATN. Also rhabdomyolysis. Proteinuria is common.
• Hantavirus is discussed on b p. 73.
Non-infective causes
• Herbal or traditional medicines are a common part of healthcare in many developing countries ( b p. 901).
• Surgical AKI:
• Incidence steadily increasing with the growth of surgical specialties and facilities across the globe.
• Includes perioperative AKI and post-operative complications.
• Trauma.
• Obstructive uropathy is increasing (ageing population, particularly ♂ ).
• Pregnancy-related AKI is declining, with fewer illegal abortions and better access to good antenatal care.
• Glucose-6-phosphate defi ciency (G6PD):
• Affects several hundred million people worldwide, mainly in the Mediterranean, Africa, Middle and Far East.
• Intravascular haemolysis occurs, following signifi cant oxidative stress (e.g. infections, drugs).
• Haemoglobinuric AKI results ( b p. 155).
• Toxins:
• Snake bites (e.g. from Elapidae, Viperidae, Colubridae, and Hydrophidae species) cause an astonishing 70% of AKI in Myanmar although much less in India (3%) and Thailand (1.2%). Venom l haemoglobinuric and myoglobinuric AKI ( b pp. 152–155), as well as ATN s to circulatory compromise and DIC (and occasional direct nephrotoxicity). Early administration of anti-venom (monovalent preferable to polyvalent) may prevent renal injury.
• Scorpion, spider, centipede, and jellyfi sh bites or stings.
• Mushroom ingestion (of Amanita , Galerina , and Cortinarius genera), associated with liver and renal failure in severe cases.
• Chemicals:
• The incidences of AKI s to poisoning with copper sulphate (leather industry), formic acid (rubber industry), and paraquat (agriculture) are now falling.
AKI in sepsis
What is the sepsis syndrome?
Sepsis accounts for 2% of all hospital admissions but 25% of admissions to ITU. AKI is a frequent complication of the sepsis syndrome, increasing in incidence as the severity of sepsis increases. Patients whose renal failure is sepsis-related have a mortality of up to 75%. With sepsis, there is evidence of (usually local) infection, with systemic signs of infl ammation ( i temp, i HR). This progresses to the sepsis syndrome if organ dysfunction ensues — typically, confusion, oliguria, hypoxia, and acidosis. Full-blown septic shock implies hypotension, despite adequate volume resuscitation, with signs of organ dysfunction.
Causes of signifi cant sepsis
• Gram +ve organisms:
• Staphylococci (incl. S. aureus , MRSA, and S. epidermidis ) 20 – 35%.
• Streptococcus pneumoniae 10%.
• Other Gram +ve 10 – 20%.
• Gram – ve organisms:
• E. coli 10 – 25%.
• Other Gram – ve (commonly Pseudomonas ) 5 – 20%.
• Others:
• Fungi ( Candida ) 3%, viruses 3%, parasites (malaria) 1 – 2%.
How sepsis becomes shock
Engulfed pathogens are lysed, liberating membrane products (including lipopolysaccharide (LPS) and exotoxin), proteins, and DNA. These frag-ments are recognized by specifi c cellular receptors (Toll-like receptors) which l NF κ -B-dependent cell activation.
Activated cells then release proinfl ammatory mediators (e.g. IL-1, TNF, IFN), stimulating local and systemic host defence networks.
Systemically activated leucocytes now orchestrate the immune response, with local leucocyte recruitment into infl amed tissue encouraged.
At the same time, anti-infl ammatory and resolution pathways (nega-tive feedback) are induced; inappropriate regulation of these pathways often leads to a deleterious prolongation of systemic infl ammation.
Within infl amed tissue, and eventually systemically, the endothelium upregulates cellular adhesion molecules and tissue factors to encourage recruitment of effector cells. Inducible nitric oxide synthase generates large quantities of NO, and the integrity of intracellular tight junctions is compromised.
The consequences are reduced microvascular fl ow and mitochondrial dysfunction, leading to organ failure.
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Clinically, this translates into
• d systemic vascular resistance (NO is a potent vasodilator and renders angiotensin II and adrenaline less effi cacious).
• i capillary leakiness (tight junctions impaired).
• Local tissue injury (neutrophil recruitment with elastase release and oxidant burst).
• i sympathetic activity.
• RAS activation:
• A2 l vasoconstriction.
• Aldosterone l Na + retention ( b pp. 456–7).
• Non-osmotic ADH (vasopressin) release l vasoconstriction.
• Vascular smooth muscle becomes less sensitive to vasoconstrictors, so, despite high circulating levels of adrenaline, angiotensin, and endothelin, the circulation remains (maximally) vasodilated.
The kidney in sepsis
• Noradrenaline l afferent arteriolar vasoconstriction l d transglomerular perfusion pressure l d GFR and Na + retention.
• i systemic NO l downregulation of intrarenal NO production l further d RBF (particularly in the metabolically vulnerable outer medulla).
• Infl ammatory cells produce oxidants and proteases that injure renal endothelium (remember 20% of cardiac output is to the kidney) l local coagulopathy with intra-glomerular thrombus formation l d capillary blood fl ow.
• The end result is d O 2 delivery and ATN ( b p. 108).
Vasopressor therapy
• Treatment with noradrenaline (NADR) acts to counteract the generalized vasodilation and sepsis associated d SVR.
• However, NADR may d RBF through the mechanism just described, thus potentiating AKI.
• In fact, available studies suggest that NADR affects renal outcome differently, depending on whether d RBF is s to sepsis-induced vasodilation or hypovolaemia.
• In sepsis, NADR has a greater effect on arteriolar resistance and can normalize renal vascular resistance, maintaining transglomerular perfusion pressure.
• NADR l i SVR l d renal sympathetic tone l i renal perfusion.
• The key point is that ‘adequate ’ fl uid resuscitation must take place before (or at least simultaneously with) vasopressor administration.