Clinical Examination of Mr Robinson - Case Study Example

PROBLEM SOLVING ASSIGNMENT - BMS2513 – January 2014 Mr Robinson is 40 years of age. He works a foreman at the local factory which for the past six months has been under the threat of closure. During this time Mr Robinson has become increasingly irritable at home and has taken to spending more time at the local pub where he drinks and smokes moderately most nights per week. In the middle of one of his working shifts a fellow worker finds Mr Robinson collapsed in the toilet. He has vomited a large quantity of blood and appears cold and clammy to the touch. The Occupational Health Staff at the factory summons an ambulance to take Mr Robinson to the local Accident and Emergency unit. Clinical Examination of Mr Robinson reveals the following. Blood pressure 80/60mmHg, Pulse 130 beats per minute (BPM) Weak and thread in character Respiratory rate: 36 breaths per minute, deep and sighing in character. He was pale with cold and clammy skin and was anxious and confused. Blood specimens analysed by the laboratory show the following. Lab Test Lab results References Serum Electrolytes Serum Sodium: 139mmol/L Serum Potassium4.5mmol/L Sodium: 135-145 mmol/L Potassium: 3.5-5 mmol/L Serum Urea & Creatinine Serum Urea: 15mmol/L Serum Creatinine: 97 µmol/L Urea: 2.5-6.7 mmol/L Creatinine: 70-150 µmol/L Full Blood Count WBC: 10.0 x10^9L Hb: 8g/dL HCT: 28 Platelet: 266 x10^9L /L WBC: 4-11 x 10^9/L HB: 13-18g/dL Hct: 42%-55% Platelet: 150-400 x10^9/L Questions: Q1. What do the clinical results reveal about this man’s present condition? Q2. How do the laboratory test results reveal about Mr Robinson’s condition? Q3. What do you conclude his diagnosis to be based on your understanding of all the results above? Q4. What other tests could House Physician carry out to strengthen the diagnosis? 1. Mr Robinson presented to the Emergency unit after vomiting massive amount of blood. His current status represents a state of hypovolemic shock which was caused by the large amount of blood in his vomit. Mild to moderate hypovolemia only leads to resting tachycardia, however blood loss of at least 50 percent results in supine hypotension (Saltzman & Fieldman 2013). The loss of blood leads to reduced intravascular volume and inadequate tissue perfusion. This causes a reduced arterial pressure and decreased tissue perfusion; hence the tissues are deprived of oxygen and nutrients (Lippincott Williams & Wilkins 2009). Mr Robinson presented with increased blood urea nitrogen suggesting renal failure due to “a large quantity of blood” in his vomiting, pointing out towards the massive reduction in intravascular volume leading to hypovolemia. The aortic and carotid receptors detect the loss of volume and increase the sympathetic activity which results in peripheral vasoconstriction and increased heart rate. The vasoconstriction causes the cold, clammy skin and the increased heart rate describes the tachycardia. Poor perfusion leads to reduced blood flow to the brain as well, leading to tissue hypoxia, which causes confusion and anxiousness. The body shifts from aerobic metabolism to anaerobic metabolism due to tissue anoxia leading to lactic acid build up and metabolic acidosis (Lippincott Williams & Wilkins 2009). Mr. Robinson’s initial presentation is consistent with the signs of hypovolemic shock and presented to the Emergency room with cold and clammy skin, tachycardia and anxiousness. His pulse was 130 beats per minute which was weak and thread in nature, exhibiting hypovolemia. As a compensatory effect, the respiratory rate is increased leading to hyperventilation, in an attempt to increase the partial pressure of oxygen in arterial blood. Mr. Robinson’s respiratory rate was 36 breaths per minute, suggesting that he was hyperventilating as a compensatory response to the metabolic acidosis. 2. Acute upper gastrointestinal bleeding can present either as blood in vomiting (hematemesis) or melena (blood in stool). In the given case, the patient presents with massive upper GI blood loss through vomiting which lead to a medically critical state of hypovolemia. Approach to diagnosis of a medical case, first revolves around the history of the patient. Age, lifestyle habits, stress and diet are important risk factors determining the course of upper GI bleeding. Hematemesis is the vomiting of bright red blood or coffee ground colored material resulting from previous bleeding, and it indicates upper GI source proximal to the ligament of Treitz (Humes 2001). In United States each year 100 patients per 10,000 are hospitalized for upper GI bleeding and about 20 patients per 100,000 are hospitalized for lower GI bleeding (Mushlin & Greene 2009). Blood specimen A of Mr Robinson exhibit the serum sodium value of 139 mmol/L, serum potassium of 4.5mmol/L, serum creatinine of 97mmol/L and Urea of 15mmol/L. Serum Sodium and Potassium: The normal serum sodium and potassium of Mr. Robinson’s blood analysis suggests that the kidney tubules have not undergone necrosis and the capability of active reabsorption and secretion of electrolytes is retained by the renal tubular cells. Any renal tubular necrosis would have resulted in deterioration of the serum electrolytes with an increase in serum potassium and decline of serum sodium. Renal tubular necrosis is presented with increased fractional sodium excretion, more than 1 percent, signifying loss of tubular function to reabsorb sodium (Tierney et al. 2008). Prerenal azotemia is characterized by increased serum creatinine to serum urea ratio, due to increased absorption of urea, but near to normal serum sodium and potassium levels as tubular function is preserved. Prerenal azotemia is caused mainly due to hypoperfusion of the kidney. The creatinine to blood urea nitrogen ratio exceeds 20:1 however, the fractional excretion of sodium is maintained at less than 1 percent (Tierney et al. 2008). Serum Urea and Creatinine: The urea is increased significantly in Mr Robinson as compared to serum creatinine which can be described as a result of prerenal azotemia and also as a consequence of absorption of nitrogenous products of blood in the small intestine (Mushlin & Greene 2009). The increased protein load in the gut leads to increased production of urea, leading to elevated serum urea levels. Increased blood urea nitrogen can also be explained because of the dehydrated status of Mr. Robinson. Normally 50 percent of the urea is reabsorbed and it is inversely related to rate of urine flow in the kidney tubules [ CITATION Mar \l 2057 ]. If the urine flow is reduced or stopped, an increased amount of urea will be reabsorbed from the tubule into the blood capillaries. In dehydrated patients, the urine flow is reduced due to low blood pressure and hypovolemia and hence these patients develop high blood urea levels. Urea reabsorption is dependent on the sodium, chloride and water reabsorption [ CITATION Mar \l 2057 ]. In dehydrated patients, the water and electrolyte absorption is increased so urea reabsorption is also increased, leading to increased blood urea nitrogen levels. Haemoglobin and Haematocrit: Mr Robinson’s laboratory analysis of blood specimen B shows haemoglobin of 8g/dL and haematocrit of 28. The initial haemoglobin in acute upper GI bleeding is often not declined as the person is losing whole blood, however, after 24 hours or more the haemoglobin declines due to dilution of blood by the extravascular fluid influx into the vascular space, a compensatory effect. Hydration can also lead to falsely low haemoglobin levels (Saltzman & Fieldman, 2013). Similarly the initial haematocrit levels are also not suggestive of the degree of blood loss and usually decrease after the exogenous and endogenous fluids have replenished the vascular space (Humes 2001). It is important to perform a peripheral blood picture in this patient to confirm chronic blood loss which would be reflected with hypochromic microcytosis and also complement the low haemoglobin and haematocrit levels. Otherwise, in a setting of acute blood loss a normocytic normochromic blood picture would be observed. Platelet Count: Thrombocytopenia is an important finding in patients with liver cirrhosis caused by alcoholism or hepatitis. Poor coagulation property is due to the inability of the liver to form coagulation factors necessary for platelet aggregation and clot formation, which lead to excessive bleeding. Total White cell count: An increased number of white blood cell count i.e. leucocytosis is also common in alcoholic hepatitis (Marsano et al. 2003). In acute GI bleeding there can be a modest rise in white cell count but not more than 15, 000/ mm^3, hence leucocytosis cannot be considered a feature of acute GI bleeding along without any infection (Mushlin & Greene 2009). The total white cell count of Mr Robinson is 10.0 x 10^9L and the platelet count is 266 x 10^9/L. The platelet count and total white blood cell analysis suggest that Mr Robinson is most probably not experiencing any liver pathology as well as no current infection associated with the acute GI bleeding. 3. In the clinical scenario presented, the most likely cause of massive blood in vomit was due to peptic ulcer bleeding which lead to hypovolemic shock and prerenal azotemia. Peptic ulcer could be preceded by significant risk factors of habitual smoking, alcohol abuse and work-related anxiety. According to the given data, it has been estimated that peptic ulcer disease was the most common cause of bleeding (60%) in the chronic alcohol abusers and alcoholic gastropathy was found in only 4% of the patients included in the study, out of which portal hypertension was the major cause of gastropathy and NSAID use was a minor cause. In actively drinking patients, peptic ulcer bleeding and disorders related to portal hypertension was presumed to be the most common causes of upper GI bleeding (Wilcox, et al., 1996). In another study, it was estimated that drinking more than 42 drinks per week increased the risk of bleeding ulcer fourfold compared with those people who drank less per week (Bak Andersen, et al., 2000). A study of 36, 656 males and females exhibited that smokers had a 2.1 fold increased risk of peptic ulcer and coffee and alcohol consumption was correlated to smoking. Although both the irritants cause the increased secretion of gastric acid but no relation to peptic ulcer prevalence could be established (Friedman, et al., 1974). Peptic ulcers can bleed without a prior history of bleeding or without previous symptoms of peptic ulcer. Ulcers usually located on the lesser curvature of the stomach or in the postero-inferior wall of the duodenum are a greater risk of massive bleeding. The reason is due to their presence in close vicinity to the large vessels and they can easily erode into the vessel (Yamada & Alpers, 2008; Norton, et al., 2001). Left gastric artery is usually affected in gastric ulcers and gastroduodenal artery in duodenal ulcers (Norton, et al., 2001). The vessel is usually present in the floor of the crater and protrudes with an aneurysmal dilation. The ulcer erodes into the lateral wall of the vessel and this leads to massive bleeding (Yamada & Alpers, 2008). Alcohol leads to increased gastric acid secretion in the stomach; however, the exact mechanism has not been explained. Alcohol also leads to gastric mucosal injury leading to inflammation, reduced prostaglandin secretion and adversely affecting the musical barriers of the stomach (Bode & Bode, 1997). Smoking is associated with increased risk of ulcer formation by increasing the duodenal load of acid and also impairs the duodenal and pancreatic bicarbonate secretion. It has also been established through studies that work related stress, post-traumatic stress, social problems and depressive symptoms increased the risk of peptic ulcers and its complications. In peptic ulcer, the defect in the gut wall extends through the muscularis mucosa into the submucosa or muscularis propria. This leads to acute wound formation due to imbalance in the musical defence barriers and acid secretion in the stomach and duodenum (Yamada & Alpers, 2009). Mr Robinson’s history, clinical symptoms, job history and the risk factors are consistent with the clinical data suggesting that the most likely cause of his bleeding was a peptic ulcer. Chronic moderate alcohol consumption is not associated with peptic ulceration; however, highly concentrated alcoholic beverages increase the risk of gastric bleeding from any previous acute lesions (Domschke & Domschke 1984). Esophageal varices are another common cause of acute upper GI bleeding in alcoholics due to cirrhotic liver disease. Varices in the esophagus and stomach are present in about half of the cirrhosis patients. Risk of spontaneous rupture is high in patients with large varices and is associated with massive blood loss, which can worsen the prognosis (Bode & Bode, 1997). However, oesophageal varices would be associated with signs of portal hypertension with laboratory findings of deranged coagulation studies, which were ruled out in the given clinical case. Other important causes of massive upper GI bleeding include gastritis caused by stress, alcohol or drugs and Mallory-Weiss tear (Friedman 2001). Erosive gastritis is also associated with alcohol intake and stress however, the patient presents with mild hematemesis due to superficial erosions and no hemodynamically significant bleeding is observed usually (Tierney, et al., 2008; (Wilson 1990). Excessive alcohol consumption also leads to alcoholic gastritis which presents with dyspepsia, nausea, emesis and minor hematemesis (Tierney, et al., 2008). Gastritis and erosions are common conditions associated with risk factors such as alcohol and smoking. Heavy acetylsalicylic acid ingestion could be associated with major bleeding or gastric ulcerations. 4. Biochemical investigations: Liver Function tests: It is important to perform liver function tests, including serum ALT and AST, to discover any underlying liver pathology caused by alcoholism. Prothrombin Time: Prothrombin time would aid in excluding any possible cause of acute GI bleeding associated with alcoholic hepatitis and cirrhosis. Non-biochemical tests: Esophago-gastro-duodenoscopy: It is the investigation of choice in upper gastrointestinal haemorrhage (Wilson, 1990; McLatchie, et al., 2007). This not only helps in locating the site of bleeding but also helps in providing therapeutic interventions such as adrenaline injection, heater probe coagulation or banding of vaices (McLatchie, et al., 2007). X-ray Films: In the history of peptic ulcer, perforation of the ulcer into the peritoneum is also an improtant and critical complication. Upright or decubitus films of abdomen should be done, which would reveal free intrapertinoneal air in 75 percent of the cases (Tierney, et al., 2008). Arteriography: This an invasive diagnostic procedure which has also become increasingly valuable and has been reported to detect the site of bleeding in 75% to 85% of cases. When used only for diagnosis, it is mostly used when endoscopy was unable to provide a satisfactory diagnosis or endoscopy was unsafe or contradindicated due to severe bleeing. However, it is rarely suitable for patients with active bleeding (Fishman, 2004). 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