Incomplete repair of the liver due to chronic diseases leads to cirrhosis, which manifests through medical conditions such as ascites, PSE, HRS, and diverse neurological changes.
Excessive retention of sodium by the kidneys due to the body’s compensatory reaction leads to an increase in hydrostatic pressure and low albumin. Another cause of ascites is the alteration of the normal mechanism for lymphatic drainage, which occurs due to fibrosis. A physician can diagnose extensive ascites through a physical examination to determine whether the patient has a bulging abdomen, which is a common observation for ascites levels exceeding 1500 milliliters (Bope, 2012). Patients with mild ascites levels, about 100militers, have to undertake an ultrasound of the abdomen to determine their condition. The main approach in managing ascites is the restriction of patients’ sodium intake to about 2 grams in a day. However, sodium restriction is only efficient in a small percentage of patients with the rest requiring the use of diuretics. The combination of spironolactone and furosemide dosage is subject to variation to sustain the patient’s electrolyte stability.
Portosystemic (Hepatic) Encephalopathy (PSE) is a syndrome that develops due to portal hypertension, which induces alteration of blood circulation from the portal system and has an association with the accumulation of nitrogenous products in the body. Diagnosis of PSE entails the revelation of characteristics such as alteration in consciousness, sleep patterns, memory, and fetor hepaticus in some patients. In addition, identification of symptoms such as lethargy and the setting in of frank coma can reveal the extent of PSE. The first step in managing PSE is the identification of a precipitating cause, which may be evident through the revelation of infection, gastrointestinal bleeding, abnormal electrolytic levels, and TIPS among other symptoms. A physician can tackle the precipitating cause using lactulose therapy, which should reverse the deterioration in cognitive and motor functions. The physician uses a nasogastric tube to administer between 15 and 30 milliliters of lactulose and should frequently evaluate the patient’s bowel movements.
Apart from PSE, neurological changes due to cirrhosis can exhibit as acquired hepatocerebral degeneration or hepatic myelopathy. Acquired hepatocerebral exhibits through signs such as dementia, ataxia, and tremor, which occur due to neuronal losses in parts of the brain such as the cerebral cortex. Hepatic myelopathy arises due to alterations in the lateral pyramidal tracts, which increase susceptibility to reduced sensory functions. Management of the two conditions requires the use of antibiotics and lactulose to prevent the buildup of excessive levels of ammonia in the blood.
Hepatorenal Syndrome (HRS)
Renal dysfunction occurs due to diverse conditions that might be evident in cirrhosis patients. Ailments such as hepatitis B and C, diabetes mellitus and immunoglobulin nephropathy lead to the development of HRS whose acuteness varies depending on factors such as diuretic, gastrointestinal bleeding, sepsis, and use of nephrotoxic medication. The primary diagnosis of HRS involves the evaluation of the creatinine levels of the patient, which should not be greater than 1.5 milligrams/deciliter for patients without signs of dehydration, infection, or usage of nephrotoxic medications. Creatinine levels greater than 2.5 milligrams/deciliter illustrate an acute type of HRS, which often arise due to gastrointestinal hemorrhage, SBP, or alcoholic hepatitis (Rakel, 1998). The treatment of HRS focuses on the reversal of renal dysfunction through medical therapy involving a combination of midodrine, octreotide, and albumin. The physician should use vasoconstrictors such as norepinephrine to improve the patient’s renal functions and plasma volume.