Acute Care

Acute Care
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ACUTE CARE 2

Liver disease
Introduction

Alcohol is a hepatotoxic compound that is commonly consumed across the globe. It is
linked to a broad range of liver associated injury, ranging from simple steatosis, fibrosis to
cirrhosis (Torruellas, French, & Medici, 2014). Alcohol liver disease refers to a spectrum of
alcohol-related injuries that are potentially reversible especially when the progression of the
disease is detected early enough. Therefore, regular screening and early diagnosis are
essential. Excessive alcohol consumption adversely affects the health of an individual and is
one of the primary causes of death in the world. Harmful or excessive use of alcohol results
in a mortality rate of up to 2.5 million and an approximate disability of adjusted life years of
up to o 69.4 million (Shield, Parry, & Rehm, 2013). As a result, it has been ranked as one of
the leading risk factors for death and disability worldwide. The toxicity of alcohol
components including ethanol largely contribute to increased chances of developing liver
disease. The liver controls most of the body support systems, therefore, a disease of the liver
is fatal as it will lead to malfunction of all the major body systems
Causes of confusion and other symptoms.
Various factors contribute to the occurrence of liver disease. Of these, duration and
amount of alcohol consumed are most significant. Host factors such as IPNPLA3 gene
polymorphisms and obesity and environmental factors also contribute to an increased risk of
developing liver disease (Singal, Chaha, Rasheed, & Anand, 2013). Disease of the liver leads
to reduced functionality of the liver which consequently cause accumulation of toxic
substances in the bloodstream. These instances lead to alterations in the level of

ACUTE CARE 3
consciousness of an individual, confusion, and other cases coma. In Mr. McGrath’s case,
hepatic encephalopathy may be the cause of disorientation.
Abdominal swelling by the patient indicates extensive complications. Life-threatening
complications associated with portal hypertension including ascites may be present in the
patient. Increased pressure on the portal vein leads to ascites characterized by fluid build-up
in the abdominal cavity. Yellowish skin, delirium, and confusion are also observed in this
condition (A.D.A.M, 2013). Varices are likely to develop in instances of portal hypertension,
as a means of providing alternative pathways for diverted blood.
Oesophageal varices pathophysiology and management strategies.
Almost half of the patients suffering from cirrhosis during diagnosis have been found
to have gastroesophageal varices (Pericleous et al., 2016). The varices arise due to portal
hypertension resulting from an increase in portal blood flow resistance in cirrhosis and also
due to the rise in blood inflow into the portal vein. An increase in resistance is said to be
structural, due to a destruction of the vascular architecture of the liver by regenerative
nodules and fibrosis as a result of an increase in the tone of the hepatic vasculature primarily
due to the dysfunction of the endothelium and a decrease in the bioavailability of nitric oxide.
Three principal events cause portal hypertension. First, it can be due to a physical
obstruction arising from a fibrosis or at other instances from regenerative nodules resulting in
an increase in the resistance to blood flow. An imbalance between vasoconstrictors and
vasodilators in the liver also develops. Such imbalance results in a reduction of the activity of
eNOS in the liver. The event is, however, rectifiable using medications such as nitrates and
beta-blockers. A combination of these events leads to the occurrence of porto-systemic
collateral circulation of aiming to decompress the portal circulation (Frazier, Stocker,
Kershner, Marasano, & McClain, 2014). Splanchnic vasodilation occurs due to a relative

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extra-hepatic and ischaemic liver increase in Nitrite Oxide, with the signalling of the sGC-
PKG and smooth muscle cell relaxation. This leads to increased blood flow volume into the
portal which maintains hypertension. This results in a hyper-dynamic circulation that is
linked to these hemodynamic variations in portal hypertension and cirrhosis. This is
manifested as high cardiac output with little arterial hypotension and systematic vascular
resistance (Pericleous, et al., 2016).
Hepatic pressure can be applied to obtain hepatic venous pressure gradient (HVPG)
that ranges normally from 1 to 5mmHg. This procedure is performed by inserting a catheter
into a hepatic vein to get the hepatic vein pressure. HVPG is equal to WHVP minus free
(HVP) where HVPG is used to represent the gradient between caval pressure and the portal
(Molina et al., 2016). FHVP acts as an internal zero by cancelling out variations in abdominal
pressure. Sinusoidal hypertension differs from pre-sinusoidal portal hypertension which
associated with an increase in HVPG as flow resistance builds up in the portal vein. Varices
therefore develop in the event that HVPG is greater than ten mmHg.
Antibiotics have been introduced in variceal hemorrhage management, a factor which
has significantly improved clinical outcomes. Bacterial infections, both primary and
secondary, are common in cirrhotic patients as bacteria actively translocate from the impaired
mucosal surface into the portal system and the patient’s impaired immune function (Molina,
Gardner, Souza-Smith, & Whitaker, 2014). In these patients, antibiotics decrease the bacterial
load, reducing infections, recurrent bleeding, and reduce morbidity and mortality in patients
with gastroesophageal varices. Broad spectrum antibiotics prophylaxis is thus recommended
in individuals with suspected and confirmed variceal hemorrhage (Shah, 2016).
Nonselective beta blockers can be used in patients having a low-risk small varices, as
they can delay variceal growth preventing variceal bleeding (Runyon, 2015, September 23).

ACUTE CARE 5
The treatment is applied in absence of severe liver disease, and where the varices are without
red wale marks. In persons with varices containing red wale marks and others associated with
a high risk of haemorrhage, non-selective beta-blockers are used.
For patients that have medium and large varices, endoscopic variceal ligation or beta-
blockers can be used. Non-selective beta-blockers are advantageous as they are cheap and use
requires no expertise. These medications also prevent against other medical conditions like
spontaneous bacterial peritonitis and bleeding from ascites and portal hypersensitive
gastropathy (Garcia-Tsao & Bosch, 2011).
The role of abdominal paracentesis and possible complications.
The presence of excess fluid in a patient’s abdominal cavity cause significant
discomfort to the patient and shortness of breath. Abdominal paracentesis is a simple
procedure that involves insertion of a needle into the peritoneal cavity of the patient to
remove the ascetic acid. Removal of a small amount of the fluid for testing is referred to as
diagnostic paracentesis, while therapeutic paracentesis is considered the removal of up to five
litres of the excess fluid so as to decrease the resultant intra-abdominal pressure helping in
relieving related abdominal pain, dyspnea and early satiety (Runyon, 2015).
Paracentesis should be performed by a properly trained physician. Performing this
procedure at the time the patient is admitted to a hospital, to patients suspected or suffering
from cirrhosis and ascites decrease the mortality rates in a health care setting. In instances
where paracentesis was conducted on admission, a lower in-hospital mortality rate was
recorded compared to those who did not perform the procedure (Cavazzo, Bugiantella,
Graziosi, Franceschini, & Donini, 2013).
Paracentesis also helps clarify the primary cause of ascites when testing for infection.
Unexpected diagnoses including chylous, eosinophilic or hemorrhagic ascites can also be

ACUTE CARE 6
indicated by this procedure (Pericleous et al., 2016). Analysis of the fluid shed light on the
cause of the ascites and if present, the bacterial infection. Upon culturing antibiotic
susceptibility of the bacteria can be identified therefore easier treatment.
Despite the benefits of paracentesis, various complications occur. The ascitic fluid
leak is the most common complication associated with the procedure. Failure to peform a Z-
track properly can lead to a leakage of the ascetic fluid leak. In this case, a large-bore needle
may be used, or when the skin incision created is overly large. If the leak on the surface is
prolonged, cellulitis may develop (Wedro, 2015).
Bleeding from a blood vessel may arise if a vein or artery is torn by the needle.
Bleeding can be extremely severe and potentially fatal especially if an artery is affected. A
further disastrous situation may arise in the presence of renal failure. In patients with primary
fibrinolysis, three-dimensional hematomas may develop requiring anti-fibrinolytic treatment
(Molina et al., 2014). Bowel infection may occur in instances where the bowel has been
injured by the paracentesis needle. Fortunately, this does not usually result to clinical
peritoritis, and thus treatment is not necessitated, not unless patients indicate signs of
infections. Death may also occur due to paracentesis.
Mr. McGrath educational requirements.
Mr. McGrath should be advice on the importance of total abstinence from alcohol to
prevent further complications. He should also be educated to take a diet low on ammonia to
reduce the amount of toxic products that will be produced by the body. High cholesterol
containing foods should also be avoided to reduce the arterial pressure and therefore amount
of fluid in the stomach. The prescribed medicine should be strictly adhered to prevent further
complications. Garcia-Tsao & Bosch, (2011) enlighten that support groups and peer help
especially from other patients and medical practitioners can be employed to provide

ACUTE CARE 7
additional moral support to patients. Sharing of past experiences by the patients will boost the
recovery of Mr. McGrath. Mr.Grath should be advised on the importance of abstinence from
cigarettes as they significantly increase the level of toxic compounds in his blood system.
Analysis of Mr. McGrath current prescription.
Propranolol or otherwise known as Inderal is prescribed to the patient for
pharmacologic crophylaxis of variceal bleeding. Varices may probably have been identified
in the patient. Propranolol reduces the portal pressure through reduction in the cardiac output,
and reducing portal blood inflow via splanchnic vasoconstriction (Runyon, 2015, September
23). Spironolactone is an aldosterone antagonist which act on the distal tubules to conserve
potassium and increase natriuresis. The drug is mainly used as a diuretic. Furosemide is
prescribed to Mr. McGrath to treat the fluid build-up in the body. The drug is an anthranilic
acid derivative and a diuretic. It inhibits absorption of sodium and chloride in the proximal,
the loop of Henle and distal tubes.
Conclusion
Alcohol liver disease is one of the primary causes of liver-related mortality in the
United States. Clinicians, therefore, should be well versed in diagnosis and treatment
procedure for the condition. Education to the population may play a significant role in
reducing severe forms of the conditions by advocating for early testing and treatment. In Mr
McGrath case, follow-up after treatment should be conducted to facilitate a full recovery. In
cases of total failure of the liver a transplant should be considered in order to maintain the
acceptable toxicity levels of blood ammonia.

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References

A.D.A.M (Ed.). (2013, December 23). Cirrhosis. Retrieved September 4, 2016, from The
New York Times:
Cavazzo, E., Bugiantella, W., Graziosi, L. A., Franceschini, M. S., & Donini, A. (2013,
February). Malignant ascites: pathophysiology and treatment. International Journal of
Clinical Oncology, 18(1), 1-9.
Frazier, T. H., Stocker, A. M., Kershner, N. A., Marasano, L. S., & McClain, C. J. (2014,
May 1). Critical pathophysiological process and contribution to disease burden.
Physiology, 203-215. Retrieved September 04, 2016
Garcia-Tsao, G., & Bosch, J. (2011, March 4). Management of varices and variceal
hemorrhage in cirrhosis. The New England Journal of Medicine, 362, 823-832.

Molina, P. E., Gardner, J. D., Souza-Smith, F. M., & Whitaker, A. M. (2014). Alcohol abuse:
Critical pathophysiological processes and contribution to disease burden. Physiology,
29, 203-215.
Pericleous, Marinos, Sarowski, Alexander, Moore, Alice, . . . Murtaza. (2016, March). The
clinical management of abdominal ascites, spontaneous bacterial peritonitis, and
hepatorenal syndrome: a review of current guidelines and recommendations.
European Journal of Gastroenterology & Hepatology, 28(3), e10-e19. Retrieved
September 04, 2016,

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Runyon, B. A. (2015, September 23). Diagnostic and therapeutic abdominal paracentesis.
Retrieved September 04, 2016, from UpToDate:

Shah, R. (2016, August 24). (P. K. Roy, Editor) Retrieved September 04, 2016, f
Shield, K. D., Parry, C., & Rehm, J. (2013). Focus on: Chronic diseases and conditions
related to alcohol use. The Journal of National Institute on Alcohol Abuse and
Alcoholism, 35(2). Retrieved September 4, 2016, Liver
transplantation in alcoholic liver diseases current status and controversies. World
Journal of Gastroenterology, 19(36), 5953-5963.
Torruellas, C., French, S. W., & Medici, V. (2014, September 7). Diagnosis of alcoholic liver
disease. World Journal of Gastroenterology, 20(33), 11684-11699.

Wedro, B. (2015, July 28). Medical treatment. (M. C. Stoppler, Editor) Retrieved September
04, 2016, from E medicine health:

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