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Alcohol-Related Liver Disease (ARLD) Case Study

2575 words (10 pages) Essay in Medical

08/02/20 Medical Reference this

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INTRODUCTION

The case study examines Edward, a 63 year old man with a history of alcohol- related liver disease (ARLD). He has deranged coagulation with an INR of 2.6 and raised transaminases. Clinically, he looks jaundiced and increasingly confused. He is oliguric and requires increasing oxygen support. The essay will briefly discuss on ARLD and the process and progression of how his symptoms came to be. It will present a detailed pathophysiology of hepatorenal syndrome (HRS) secondary to liver disease and will focus on the medical and nursing management of HRS type 1 (HRS-1).

BACKGROUND

  Edward’s case appears to be an acute on chronic liver disease secondary to ARLD. Alcohol- related liver disease (ARLD) is defined as an injury to the liver as a result of excessive consumption of alcohol; and it has a spectrum of complex signs and symptoms depending on the stage and severity of the liver damage (Rehm et al., 2013). Ethanol undergoes hepatic metabolism and is converted to acetaldehyde, the main mediator of alcohol damage in the liver tissues ranging from fatty changes, inflammation to fibrosis (Sheron et al., 2012). His elevated INR signifies that his synthetic liver function has been compromised. Hepatocytes are involved in the synthesis of most blood coagulation factors, subsequently an abnormality in the INR will imply an acute liver damage as the shortest half-life of clotting factors averagely ranges from 3-6 hours (Schneider, 2004). The raised transaminases, Alanine aminotransferase (ALT) and Aspartate aminotransferase (AST), signifies that there is an ongoing hepatocyte damage since transaminases are produced in the liver, skeletal and cardiac muscles when there is injury. ALT is primarily leaked out in the general circulation when hepatocytes are injured, but AST is also raised when the injury is due to ethanol (Salermo et al., 2007). The jaundice is caused by raised bilirubin levels and shows that the excretory function of the liver is affected. Unconjugated bilirubin (UB) is produced from the breakdown of red blood cells; it then binds with albumin and is converted by glucuronyl transferase in the liver to conjugated bilirubin (CB) that is water-soluble and is easily excreted in the bile (Nadim et al., 2016). Damage to the hepatocytes reduces the ability of the liver to convert UB to CB consequently raising serum levels of bilirubin, causing the yellow discoloration of the skin and mucous membranes. The confusion is secondary to the elevated ammonia levels due to liver insufficiency. Ammonia is a toxic alkaline substance that is a byproduct of protein metabolism, and the liver converts the ammonia to urea so that it can be easily excreted in the urine via the kidneys (Rivolta et al., 1998). If there is an inadequacy in the liver to clear ammonia, it accumulates in the bloodstream, eventually disturbing brain function; this is known as hepatic encephalopathy (HE) which presents as a wide spectrum of neurological, metabolic and psychiatric abnormalities in the exclusion of any other brain pathology (Sharma, 2009). The increasing oxygen requirements is the beginning of hepatopulmonary syndrome (HPS) which is characterized by intrapulmonary vascular dilatation and arterial hypoxemia due to the liver’s inability or limited function to clear out and inactivate inflammatory and vasoactive mediators secondary to portal hypertension and shunting (Zardi et al., 2009). The ongoing HE also contributes to this symptom. The decreasing urine output is a late sign of hepatorenal syndrome (HRS). HRS, in the absence of any known renal pathology, is a reversible functional renal impairment that occurs in patients with advance liver disease or severe fulminant liver injury (Henriksen et al., 1994). There is a 10% occurrence of HRS in cirrhotic patients regardless of sex. Patients with decompensated cirrhosis have almost 20% likelihood of developing HRS and doubles the probability in 5 years. And almost half of end-stage cirrhotics will be affected with HRS (Carvalho et al., 2012).

PATHOPHYSIOLOGY OF HRS

HRS is the result of the vasoconstriction of the renal vascular bed. The pathophysiology of HRS begins with the structural and dynamic changes secondary to liver cirrhosis which include: fibrosis, angiogenesis, vascular occlusion, and nodule formation subsequently initiating an increase in the intrahepatic resistance to portal blood flow termed as portal hypertension (PH) (Zardi et al., 2013).  Numerous compensatory mechanisms are attempted by the body to counter and adapt to the PH but consequently making the pre-existing clinical condition worse.

PH triggers the hepatorenal reflex to stimulate the sympathetic nervous system (SNS) directly leading to renal vasoconstriction, decrease renal blood flow and an increase sodium reabsorption (Wadei et al., 2006). To offset this reflex, a rise in splanchnic production of vasodilators causes splanchnic vasodilatation (SV), the key pathophysiological feature of HRS. SV consequently lessens the arterial blood flow and circulation, thus dropping the blood pressure (BP); the fall in pressure stimulates the carotid baroreceptors, triggering further the SNS. Moreover, the renin- angiotensin- aldosterone (RAA) system is activated due to the hypotension which will promote further sodium and water reabsorption from the kidneys. Furthermore, the circulating angiotensin-II and SNS stimulation initiates vasopressin release which causes vasoconstriction in the renal vascular bed and water retention. In the long run, the body develops an autonomic neuropathy that makes the splanchnic bed less responsive to circulating vasoconstrictors promoting more splanchnic vasodilatation. Another mechanism in response to PH is the formation of portosystemic shunts such as gastroesophageal varices, splenogastric shunts and splenorenal shunts. Theses shunts function to divert a large quantity of portal blood flow away and bypass the liver secondary to the increasing intrahepatic pressures. In this way, a number of vascular mediators that causes renal vasoconstriction such as thromboxane, endotoxins, endothelin and neurotransmitters avoid being inactivated from the hepatic metabolism, thus increasing levels worsens the renal vasoconstriction (Angeli and Merkel, 2008). In contrast, vasodilators such as prostacyclin, vascular endothelial growth factor and nitric oxide (NO) is produced in cirrhosis as a result of up-regulation of endothelial NO synthase activity from the increased shear stress on splanchnic and systemic circulation; NO in HRS decreases systemic vascular pressure and increase renal vasoconstriction (Moller and Bendtsen, 2015). The bypassing of these mediators from liver metabolism contributes to more splanchnic vasodilation. Finally, an elapsing event, such as a rapid fluid loss due to bleeding or excessive diuresis; an increased vasodilatation due to medications; and exaggerated systemic inflammatory response due to infection may add and favor the perpetuation of this trigger (Francoz et al., 2016).

The pathophysiological process of HRS has four main features including: (1) increase renal vasoconstriction (2) drop in glomerular filtration rate (GFR) (3) rise in creatinine and (4) impaired sodium and water excretion consequently a decline or cessation of urine production. Edward’s acute presentation in the A & E signifies the possibility of him developing HRS type 1 rather than HRS type 2 because aside from the acuity, the major clinical feature of the latter which is ascites that is resistant to diuretics is not present (Arroyo et al., 2008). His oliguria is a late sign of HRS.  Studies show that urine output may exceed 400 ml daily, with significantly lower output being observed only within a few days from death (Esrailian et al., 2007). Since the availability of his medical history is minimal, comparison of baseline creatinine to the present one is essential to diagnose HRS-1. Doubling of serum creatinine level greater than 2.5mg/dl in less than 2 weeks is essential to diagnose it (Pandey et al., 2014). It is also beneficial to exclude the presence of shock; existing use of nephrotoxic medications or any other parenchymal kidney disease (Arroyo et al., 2008). HRS is an independent risk factor for a poor prognosis in patients with acute-on-chronic liver failure (Zhang et al., 2016) and without treatment, cirrhotics with HRS-1 have a median survival of 2 weeks, with a few patients surviving >10 weeks, thus, it is very important to address his evolving HRS as it is reversible if caught and treated early on. (Salerno et al., 2011). On the other hand, his other signs of acute deterioration such as the coagulopathy, jaundice, confusion and oxygenation problems is all related from an acute decompensation of his chronic ARLD triggered possibly by infection, malnutrition, ethanol usage, drug toxicity, ascites, or stress. The insult that caused this acute decompensation has to be investigated as it is not a single organ illness but a complex multi- system disorder (Pearson and Thomson, 2018).

MEDICAL/ SURGICAL MANAGEMENT OF HEPATORENAL SYNDROM TYPE 1

The acuity of Edward’s symptoms necessitates admission to a critical care unit for close monitoring. The management of HRS ranges from pharmacological treatment, renal replacement therapy (RRT), and surgical management, but the definitive treatment is liver transplantation. All treatment modalities are impermanent and is done just to bridge for liver transplantation (source).

The goal of pharmacologic treatment is to counteract the key pathophysiological process of HRS-1, the splanchnic vasodilation (SV).  These pharmacologic interventions to improve the renal function does not affect the underlying liver disease (Mindikoglu and Pappas, 2018). A vasopressin analogue, Terlipressin is considered the first-line vasoconstrictor in the treatment of HRS. It is given to activate receptors in the smooth muscle cells in the splanchnic vascular bed to constrict, counteracting splanchnic dilatation and returning the volume to the peripheral circulation. The combination of Terlipressin and albumin has been shown to decrease the RAA activity along with the improvement in GFR (Wong and Blendis, 2001). In contrary, a recent meta-analysis by Gifford et al. (2017), evaluated that Terlipressin was significantly superior to placebo with or without albumin. Midodrine is an alpha-adrenergic vasoconstrictor that constricts splanchnic vessels which reverses partially the effects of HRS. As a sole therapy, it is not effective, but when combined with albumin and octreotide, an improvement on MAP, renal function, refractory ascites and plasma renin activity is observed. Octreotide contributes by inhibiting glucagon, which causes splanchnic dilatation (Wadei, 2012). Noradrenaline is a catecholamine that is an alternative to Terlipressin. It is an alpha-adrenergic activity reverses the splanchnic dilatation improving urine output, sodium excretion, serum sodium concentration, creatinine clearance, MAP and RAA activity (Davenport A. et al., 2012).

It is suggested by O’Leary et al. (2016), that Albumin should be given in combination with any vasoconstrictor drug regimen for the therapy to be more effective. Sadly, comparing the 3 vasoactive drugs, none of them showed any significant mortality reduction because it does not treat the underlying liver disease (Mattos et al., 2016).

Renal replacement therapy (RRT) is indicated in uremia, metabolic decompensation and electrolyte balance or volume overload. It is initiated for patients awaiting liver transplantation or when improvement to liver function is expected and this modality also aids in upgrading the patient’s priority in the transplant process (Baraldi et al., 2015). Molecular absorbent recirculating system (MARS) is used to eliminate albumin-bound toxins that damages the hepatocytes thereby improving organ function (Achim et al., 2014). RRT and MARS will also help with clearing out the ammonia, bilirubin, inflammatory and vascular mediators, thus improving Edward’s HE, HPS, HRS and jaundice.  A prospective, randomized, controlled trial by Banares et al. (2014), showed that patients with HRS-1 treated with MARS, RRT and standard medical treatment has a significant reduction in creatinine and mortality compared to RRT and standard medical treatment alone.

Transjugular Intrahepatic Portosystemic shunting (TIPS) is a surgical procedure utilized for treatment of complication of PH to prevent blood from the gastrointestinal system to go directly to the heart and surpass the liver, reducing PH (Fabrizi et al., 2013). It is generally contraindicated in patients with unresolved HRS-1 but it is shown to reduce the risk of HRS in patients with cirrhosis and diuretic-refractory ascites (Gines et al., 2002).

Liver transplantation is the definitive treatment for HRS-1. It has been observed that AKI improves and renal function normalizes after liver transplant, therefore, a liver-renal transplant is not recommended (Shah, N., 2016). Outcomes of patients with HRS post-liver transplant showed a 76% renal recovery rate and 97% 1-year survival rate (Wong et al., 2015).

The goal of nursing care is to provide a close hemodynamic monitoring as Edward can deteriorate rapidly. In addition, he is also on vasoactive medications that has a wide range of adverse effects. Routine checks on his electrolytes, coagulation and biochemistry is necessary to see the trends and progress, and correcting any abnormalities as it arise. He should be evaluated for transplantation and if possible, transferred to a specialist hospital that manages liver diseases and transplants. If his condition improves, he should be referred to Drug and Alcohol Rehabilitation Team (DART) and social worker to assess his support system and living condition. If his condition does decline, he should be referred to palliative and spiritual care.

CONCLUSION

HRS is reversible and has a high mortality rate, early diagnosis and prompt treatment is the key for patient survival. The management for HRS is mostly supportive just to bridge for liver transplantation.

REFERENCES

  • Angeli, P. and Merkel, C. (2008) Pathogenesis and management of hepatorenal syndrome in patients with cirrhosis, Journal of Hepatology, 48(1), pp. 93-103
  • Arroyo, V., Fernandez, J., and Gines, P. (2008) Pathogenesis and treatment of hepatorenal syndrome. Seminars in Liver Disease, 28(1), pp. 88-95
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  • Pearson, J. and Thomson, E. (2018) Decompensated liver cirrhosis, Anaesthesia and intensive care medicine, pp. 101-106
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