Screening for Hepatic and Biliary Disease

Chapter 9

Screening for Hepatic and Biliary Disease

As with many of the organ systems in the human body, the hepatic and biliary organs (liver, gallbladder, and common bile duct) can develop diseases that mimic primary musculoskeletal lesions (Fig. 9-1). The musculoskeletal symptoms associated with hepatic and biliary pathologic conditions are generally confined to the mid-back, scapular, and right shoulder regions. These musculoskeletal symptoms can occur alone (as the only presenting symptom) or in combination with other systemic signs and symptoms discussed in this chapter.

Hepatic and Biliary Signs and Symptoms

The major causes of acute hepatocellular injury include hepatitis, drug-induced hepatitis, and ingestion of hepatotoxins. The physical therapist is most likely to encounter liver or gallbladder diseases manifested by a variety of signs and symptoms outlined in this section.

Taking a careful history and making close observations of the client’s physical condition and appearance can detect telltale signs of hepatic disease. Most of the liver is contained underneath the rib cage and is largely inaccessible (Fig. 9-2). An enlarged liver that is palpable is always a red flag (see Fig. 4-51). Medical diagnosis of liver or gallbladder disease is made by x-ray examination or ultrasonic scanning of the gallbladder and computed tomography (CT) scanning of the abdomen, including the liver.

Other tests, such as a cholescintigraphy, may be used to track the flow of radioactivity into and out of the gallbladder to confirm gallstones. Blood tests may be used to look for signs of infection, obstruction, or jaundice. Laboratory tests useful in the diagnosis and treatment of liver and biliary tract disease are listed inside the back cover.

Skin and Nail Bed Changes

Skin changes associated with impairment of the hepatic system include jaundice, pallor, and orange or green skin in a Caucasian individual. Change in skin tones may be visible in Black or Asian people, but these may only be observable to the affected individual or to those who know him or her well. In some situations jaundice may be the first and only manifestation of disease. It is first noticeable in people of all skin colors in the sclera of the eye as a yellow hue when bilirubin reaches levels of 2 to 3 mg/dL. When the bilirubin level reaches 5 to 6 mg/dL, changes in skin color occur.

Other skin changes may include pruritus (itching), bruising, spider angiomas (Fig. 9-3), and palmar erythema (see Fig. 9-5). Spider angiomas (arterial spider, spider telangiectasis, vascular spider), branched dilations of the superficial capillaries resembling a spider in appearance (Fig. 9-4), may be vascular manifestations of increased estrogen levels (hyperestrogenism). Spider angiomas and palmar erythema both occur in the presence of liver impairment as a result of increased estrogen levels normally detoxified by the liver.

Palmar erythema (warm redness of the skin over the palms, also called liver palms), caused by an extensive collection of arteriovenous anastomoses, is especially evident on the hypothenar and thenar eminences and pulps of the finger (Fig. 9-5). The person may complain of throbbing, tingling palms. The soles of the feet may be similarly affected. Throbbing and tingling may be associated with these anastomoses.

Various forms of nail disease have been described in cases of liver impairment such as the white nails of Terry (Fig. 9-6). Other nail bed changes, such as white bands across the nail plate (leukonychia), clubbed nails (see Fig. 4-36), or koilonychia (see Fig. 4-32), can occur, but these are not specific to liver impairment and can develop in the presence of other diseases as well.

Musculoskeletal Pain

Musculoskeletal pain associated with the hepatic and biliary systems includes thoracic pain between the scapulae, right shoulder, right upper trapezius, right interscapular, or right subscapular areas (see Fig. 9-10 and Table 9-1).

Referred shoulder pain may be the only presenting symptom of hepatic or biliary disease. Afferent pain signals from the superior ligaments of the liver and the superior portion of the liver capsule are transmitted by the phrenic nerves. Sympathetic fibers from the biliary system are connected through the celiac (abdominal) and splanchnic (visceral) plexuses to the hepatic fibers in the region of the dorsal spine (see Fig. 3-3).

The celiac and splanchnic connections account for the intercostal and radiating interscapular pain that accompanies gallbladder disease. Although the innervation is bilateral, most of the biliary fibers reach the cord through the right splanchnic nerves, synapsing with adjacent phrenic nerve fibers innervating the diaphragm and producing pain in the right shoulder (see Fig. 3-4).

Hepatic osteodystrophy, abnormal development of bone, can occur in all forms of cholestasis (bile flow suppression) and hepatocellular disease, especially in the alcoholic person. Either osteomalacia or more often, osteoporosis frequently accompanies bone pain from this condition. Vertebral wedging, vertebral crush fractures, and kyphosis can be severe; decalcification of the ribcage and pseudofractures1 occur frequently.

Pseudofractures, or Looser’s zones, are narrow lines of radiolucency (areas of darkness on x-ray film), usually oriented perpendicular to the bone surface. This may represent a stress fracture that is repaired by laying down inadequately mineralized osteoid, or these sites may occur as a result of mechanical erosion caused by arterial pulsations, since arteries frequently overlie sites of pseudofractures.

Osteoporosis associated with primary biliary cirrhosis and primary sclerosing cholangitis parallels the severity of liver disease rather than its duration. Painful osteoarthropathy may develop in the wrists and ankles as a nonspecific complication of chronic liver disease. Rhabdomyolysis is a potentially fatal condition is which myoglobin and other muscle tissue contents are released into the bloodstream as a result of muscle tissue disintegration. This could occur with acute trauma (e.g., crush injuries, significant blunt trauma, high-voltage electrical burns, surgery2), severe burns, overexertion,3 or in the case of liver impairment, from alcohol abuse or alcohol poisoning or the use of cholesterol-lowering drugs called statins (e.g., Zocor, Lipitor, Crestor, Mevacor, Pravachol).4

Rhabdomyolysis is characterized by muscle aches, cramps, soreness, and weakness. It may be accompanied by other symptoms of respiratory muscle myopathy (impaired diaphragmatic function)5 or liver or renal involvement. Laboratory testing will show a creatine kinase (CK) level more than 10 times the upper limit of normal.

Although the literature reports the incidence of this severe myopathy with statin use as about 0.1% to 2.0% in clinical trials,6 therapists (and others) report seeing cases more often than the low percentage would suggest. Any anatomic region can be affected, but the back and extremity musculoskeletal pain are the two areas of involvement reported most often.7,8

Statin-associated myopathy appears to occur more often in people with complex medical problems and/or those taking illegal drugs (e.g., cocaine, heroin, LSD) or abusing prescription drugs (e.g., barbiturates and amphetamines).9 Other risk factors that increase the chances of this condition include excessive alcohol use, advancing age (over 80 years), recent history of surgery, and small physical stature.4 For additional discussion, see Screening for Side Effects of Statins in Chapter 6.

Neurologic Symptoms

Neurologic symptoms, such as confusion, sleep disturbances, muscle tremors, hyperreactive reflexes, and asterixis, may occur. When liver dysfunction results in increased serum ammonia and urea levels, peripheral nerve function can be impaired.

Ammonia from the intestine (produced by protein breakdown) is normally transformed by the liver to urea, glutamine, and asparagine, which are then excreted by the renal system. When the liver does not detoxify ammonia, ammonia is transported to the brain, where it reacts with glutamate (excitatory neurotransmitter), producing glutamine.

The reduction of brain glutamate impairs neurotransmission, leading to altered central nervous system (CNS) metabolism and function. Symptoms of poor concentration, fatigue, and other symptoms of encephalopathy can result.

Another outward sign of liver disease producing CNS dysfunction is asterixis. Impaired inflow of joint and other afferent information to the brainstem reticular formation produces this movement dysfunction. Also called flapping tremors or liver flap, asterixis is described as the inability to maintain wrist extension with forward flexion of the upper extremities. It is tested by asking the client to actively hyperextend the wrist and hand with the rest of the arm supported on a firm surface or with the arms held out in front of the body (Fig. 9-7).10 The test is positive if quick, irregular extensions and flexions of the wrist and fingers occur. Asterixis may also be observed when releasing the pressure in the arm cuff during blood pressure readings.

Asterixis and numbness/tingling (the latter are misinterpreted as carpal tunnel syndrome) can occur as a result of this ammonia abnormality, causing an intrinsic nerve pathologic condition (Case Example 9-1). There are many potential causes of carpal tunnel syndrome, both musculoskeletal and systemic (see Table 11-2). Careful evaluation is required (Box 9-1).

A careful history and close observation of the client are important in determining whether a person may need a medical referral for possible liver disease. Jaundice in the postoperative client is not uncommon, but it can be a potentially serious complication of liver damage that occurs following surgery and anesthesia. Clues to screening for hepatic disease (see Clues to Screening for Hepatic Disease at the end of this chapter) should be taken into consideration when evaluating the clinical history and observations.

Gastrointestinal System

Normally, bilirubin, excreted in bile and carried to the small intestines, is reduced to a form that causes the stool to assume a brown color. Light-colored (almost white) stools and urine the color of tea or cola indicate an inability of the liver or biliary system to excrete bilirubin properly. Gallbladder disease, hepatotoxic medications, or pancreatic cancer blocking the bile duct may cause light stools.

Clinical Signs and Symptoms

Liver Disease


• Dark urine and light-colored or clay-colored stools

• Ascites (Fig. 9-8)

• Edema and oliguria (reduced urine secretion in relation to fluid intake)

• Right upper quadrant (RUQ) abdominal pain

Hepatic and Biliary Pathophysiology

Liver Diseases


Hepatitis is an acute or chronic inflammation of the liver. It can be caused by a virus, a chemical, a drug reaction, or alcohol abuse. In addition, hepatitis can be secondary to disease conditions, such as an infection with other viruses (e.g., Epstein-Barr virus or cytomegalovirus).

Viral Hepatitis: Viral hepatitis is an acute infectious inflammation of the liver caused by one of the following identified viruses: A, B, C, D, E, and G (Table 9-2).

Hepatitis is a major uncontrolled public health problem for several reasons: not all the causative agents have been identified, there are limited specific drugs for its treatment, its incidence has increased in relation to illicit drug use, and it can be communicated before the appearance of observable clinical symptoms.

Viral hepatitis is spread easily to others and usually results in an extended period of convalescence with loss of time from school or work. It is estimated that 60% to 90% of viral hepatitis cases are unreported because many cases are subclinical or involve mild symptoms.11,12

Hepatitis A and E are transmitted primarily by the fecal-oral route. Common source outbreaks result from contaminated food or water. Hepatitis A virus (HAV) must also be considered a potential problem in situations where fecal-oral communication along with food handling and/or unsanitary conditions occur. Some examples of potential sources of contact with HAV might include restaurants, day care centers, correctional institutions, sewage plants, and countries where these viruses are endemic.13,14

Hepatitis viruses B, C, D, and G are primarily bloodborne pathogens that can be transmitted from percutaneous or mucosal exposures to blood or other body fluids from an infected person.

Hepatitis B virus (HBV) is usually transmitted by inoculation of infected blood or blood products or by sexual contact and is also found in body fluids (e.g., spinal, peritoneal, pleural), saliva, semen, and vaginal secretions. Hepatitis D virus (HDV) must have HBV present to coinfect. Groups at risk include homosexuals and intravenous (IV) drug users; health care workers in any area in which contact with blood, blood products, or body fluids is likely; and residents and workers in correctional settings.14,15

Hepatitis C virus (HCV) is transmitted similarly to HBV and HDV. Risk factors are also very similar with the addition of people who have received blood transfusions or organ transplants, including anterior cruciate ligament (ACL) reconstruction allograft.16,17 There has been growing concern worldwide about the risk of occupational transmission of HCV.

Occupational exposure to HCV accounts for approximately 4% of new infections. On average, the chance of acquiring HCV after a needle-stick injury involving an infected patient is 1.8% (range, 0% to 7%). Reports of HCV transmission from health care workers to patients are extremely uncommon.14

Hepatitis G virus (HGV) designation has been applied to a virus that is percutaneously transmitted and associated with bloodborne viral presence lasting approximately 10 years. HGV has been detected primarily in IV drug users, clients on hemodialysis, clients with hemophilia, and in a small percentage of blood donors. It does not appear to cause important liver disease or affect the response rate of those with chronic HBV or HCV to antiviral therapy.18

Hepatitis affects people in three stages: the initial or preicteric stage, the icteric or jaundiced stage, and the recovery period (Table 9-3). During the initial or preicteric stage, which lasts for 1 to 3 weeks, the person experiences vague gastrointestinal (GI) and general body symptoms. Fatigue, malaise, lassitude, weight loss, and anorexia are common.

Many people develop an aversion to food, alcohol, and cigarette smoke. Nausea, vomiting, diarrhea, arthralgias, and influenza-like symptoms may occur. There is a strong association between hepatitis-induced arthralgia and age with increasing incidence of joint involvement with increased age; arthralgia in children is much less common.19,20 The liver becomes enlarged and tender (see Fig. 4-51), and intermittent itching (pruritus) may develop. From 1 to 14 days before the icteric stage, the urine darkens and the stool lightens as less bilirubin is conjugated and excreted.

The icteric (acute) stage is characterized by the appearance of jaundice, which peaks in 1 to 2 weeks and can persist for 6 to 8 weeks. During this stage, the acuteness of the inflammation subsides. The GI symptoms begin to disappear, and after 1 to 2 weeks of jaundice the liver decreases in size and becomes less tender. During the icteric stage the post-cervical lymph nodes and spleen are enlarged (see Fig. 4-53). Persons who have been treated with human immune serum globulin (ISG) may not develop jaundice.

The recovery stage lasts for 3 to 4 months, during which time the person generally feels well but fatigues easily.

People with mild-to-moderate acute hepatitis rarely require hospitalization. The emphasis is on preventing the spread of infectious agents and avoiding further liver damage when the underlying cause is drug-induced or toxic hepatitis. People with fulminant (sudden and severe or prolonged) hepatitis require special management because of the rapid progression of their disease and the potential need for urgent liver transplantation.

An entire spectrum of rheumatic diseases can occur concomitantly with HBV and HBC, including transient arthralgias, vasculitis, polyarteritis nodosa, rheumatoid arthritis (RA), fibromyalgia, lymphoma, Sjögren’s syndrome, and persistent synovitis. Some conditions, such as RA and fibromyalgia, occur only in association with HCV, whereas others, such as polyarteritis nodosa, are observed in association with both forms of hepatitis.20-22

Rheumatic manifestations of hepatitis are varied early in the course of disease and can be indistinguishable from mild RA. The therapist should be suspicious of anyone with risk factors for hepatitis, including injection drug use; previous blood transfusion, especially before 1991; hemodialysis; or other exposure to blood products/body fluids, such as a health care worker (Box 9-2), or a past history of hepatitis that currently appears with arthralgias (Case Example 9-2).

Other red flag symptoms include joint or muscle pain that is disproportionate to the physical findings and the presence of palmar tendinitis in someone with RA and positive risk factors for hepatitis.

Chronic Hepatitis: Chronic hepatitis is the term used to describe an illness associated with prolonged inflammation of the liver after unresolved viral hepatitis or associated with chronic active hepatitis (CAH) of unknown cause. Chronic is defined as inflammation of the liver for 6 months or more. The symptoms and biochemical abnormalities may continue for months or years. It is divided into CAH and chronic persistent hepatitis (CPH) by findings on liver biopsy.

Chronic Active Hepatitis: This type of hepatitis refers to seriously destructive liver disease that can result in cirrhosis. CAH is often a result of viral infection (HBV, HCV, and HDV), but it can also be secondary to drug sensitivity (e.g., methyldopa [Aldomet], an antihypertensive medication, and isoniazid [INH], an antitubercular drug).

Steroid therapy is sometimes recommended for clients with evidence of aggressive liver inflammation and necrosis (identified by liver biopsy) as a result of these drugs. If CAH is left untreated, its course is unpredictable and may range from progressive deterioration of liver function to spontaneous remissions and exacerbations.

Steroids may be used to treat CAH. They are usually prescribed for a period of 3 to 5 years. In addition, recombinant interferon-alpha-2b injections in low doses over a 6-month period have been shown to improve hepatic function in persons with CAH. Treatment of HCV is relatively new and consists of the use of interferons (IFNs), a protein naturally occurring in the healthy body in response to infection such as the hepatitis virus.

Conventional IFN has been used for many years in the treatment of chronic HCV in clients who persistently maintain HCV/RNA blood levels. Combining IFNs with the drug ribavirin has resulted in better control of chronic HCV in some individuals, but the treatment is not well tolerated because of side effects from the ribavirin.23,24

Pegylated IFNs, such as Pegasys (peginterferon alpha-2a), are improved forms of IFNs that allow a decrease in dosage and offer improved efficacy. Peginterferons (PEGs) in combination with ribavirin are now considered the standard treatment for chronic HCV infection. These new PEG interferons do not eliminate the known side effects associated with classical interferon treatment (e.g., fatigue, headache, myalgia, fever, anxiety, irritability, GI upset).19,25

Mar 20, 2017 | Posted by in MANUAL THERAPIST | Comments Off on Screening for Hepatic and Biliary Disease
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