ANTY 3400 Charteris Assignment 1

Student Name: Adam Student Number: 100312428

Ian is a 47 year male who works on an assembly line at an auto parts manufacturer. He was helping back up a forklift. The forklift driver was not paying attention and injured Ian by crushing his left leg in between the forklift and another piece of machinery. As a result, his left leg was crushed to the level of the mid-shaft femur. The wound did not seem to be bleeding significantly but Ian was in a great deal of pain and obviously terrified that he is going to lose his arm. Paramedics were called and Ian was transported to hospital. In the next couple of days, Ian suffered from two life threatening complications of his injury. He survived but eventually his leg was amputated and he was forced to adjust to life without his left leg. a. During his second day in hospital, Ian suffered from an episode of extreme bradycardia that was the direct result of the injuries that he sustained. Describe the mechanism by which his crush injury could have caused his bradycardia.

The pathology behind Ians bradycardia begins with the crush injury he sustained. The muscle in the region where the pressure from the forklift is applied becomes damaged causing the intracellular contents of the compressed and damaged muscle to be released into the interstitial spaces. The muscles in his leg are separated by thick fascia that envelop nerves, blood vessels and muscle (Porth et. Al 84). When Ians leg is crushed, trauma to the leg causes swelling and increases the pressure within each area enveloped by fascia called a compartment. Eventually the pressure increases until blood is no longer able enter the compartment to supply the muscle with oxygen. In the absence of circulation, toxic metabolites and by products of cellular respiration accumulate in the region distal to the compressed region of tissue as well. With the myocytes dead or damaged, there is a large efflux of previously intracellular potassium into the blood stream once perfusion is restored. This potassium eventually reaches the heart where it suppresses the rate of contraction by inhibiting depolarization of the pacemaker cells and cardiac muscle. While hyperkalemia primarily effects phase three of the cardiac action potential, resulting in the characteristic peaked T waves seen on ECG monitors, it is hyperkalemias effect on resting membrane potential that gives rise to decreased conduction speed (Parham and Barham). Since it is potassium that is primarily responsible for the resting membrane potential, as it can leak out of the cell, when potassium levels outside the cell increase, the intracellular levels of potassium also increase due to reduced tendency to leave the cell with higher concentrations present in the interstitial space. This brings the resting membrane potential closer to 0. (See Fig 1., dotted line represents hyperkalemic cardiac action potential) b.

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ANTY 3400 Charteris Assignment 1 c. d.

Student Name: Adam Student Number: 100312428 Fig. 1 Texas Heart Institute Journal 2006; 33(1): 4047.

According to Parham et. al of the St. Louis School of Medicine, higher concentrations of intracellular potassium caused by hyperkalemia decreases the speed at which sodium enters the cell. It is the increased duration of phase zero as seen in Fig 1 that eventually gives rise to the decreased speed of conduction and rate of contraction seen in the patient above (bradycardia). In the second possible pathology, the widespread dilatation of blood vessels within the leg due to the release of intracellular potassium facilitates stagnation of blood and the formation of a deep vein thrombosis. It is entirely possible that this thrombus became embolic and entered a branch of the coronary arteries nourishing the sinoatrial node causing it to die and forcing other autorhythmic portions of the heart to take over which have a slower intrinsic rate of firing that the damaged sinoatrial node.

b. Ian survives the bradycardia, but later that evening he goes into renal failure and almost dies again. This time it takes several days to resolve the problem. Describe the mechanism by which his crush injury could have caused his renal failure.

So this time I will start of my answer from the point we discussed above where a crushing injury caused the release intracellular contents. Myoglobin is a protein present in the muscles normally used for oxygen storage. When the intracellular contents of the muscle are excreted into the blood stream, the myoglobin contained in the muscle eventually reaches the kidneys (Vanholder et. al). At this point myoglobin has three mechanisms of action that damage the kidney. First of all it induces renal hypoperfusion, this is due to the fact that myoglobin is a potent inhibitor of nitric oxide, an important vasodilator (Malik). The second mechanism involves how myoglobin is broken down and filtered by the kidneys. After myoglobin is filtered from the blood by the glomerulus, it is broken down by lysosomes in the proximal tubules (Malik). After myoglobin is broken down into globulin and ferrihemate, ferrihemate is transported out of the tubular cell at the cost of one ATP molecule. This expenditure of energy is toxic to the tubular cells in the presence of high concentrations of ferrihemate. Thirdly these myoglobin proteins and desquamated tubular cells accumulate in the tubules obstructing and inihibiting the filtration of other substances in the blood (Malik). In the presence Page 2 of 8

ANTY 3400 Charteris Assignment 1

Student Name: Adam Student Number: 100312428 of excess myoglobin and insufficient renal perfusion, the kidneys energy stores are taxed to the point where the tubular cells become damaged, the tubules become clogged and renal failure begins.

You are attending to Bill, a 27 year old patient. Bill was driving his car a 60 kph when he swerved to avoid a pedestrian and his car struck a telephone pole, knocking it over. It happened so fast that he didnt even have time to brake. Bill was wearing his seat belt and the airbag did deploy. He doesnt really remember what happened, but then it all happened so fast. Bill tells you that he has vague pain all over his abdomen. It is very hard for him to describe the pain. On physical examination you note diffuse abdominal tenderness but no distension. While you complete your assessment, your partner administers oxygen and obtains vital signs. The fire fighters assist you with immobilization. At this time, Bills pulse is 128 full and regular and his blood pressure is 90/60. His skin is cool, pale and slightly diaphoretic (there are no sweat lines) and he is breathing at 28 breaths per minute, laboured but with good clear air entry bilaterally to the bases. Bill is oriented to person, place and time and has short and long term memory. a. List seven different potentially life-threatening abdominal injuries that Bill may have sustained. The following seven potentially life threatening injuries may have occurred: Injury to the spleen, laceration of the liver along the ligamentum teres hepatis, injury to the kidney, perforated bowel, ruptured or lacerated pancreas, trauma to the bladder or diaphragmatic rupture. It is important to note that all of these may present with little or no abdominal distension initially. b. What is the life threat associated with each? How long would it take for the life threat to develop?
Injury Injury to the Spleen Laceration of the liver Life Threat Rupture of the Spleen causing massive hemmorage from the essels supplying the spleen hypovolemia and death. (Ruptured Spleen) Rapid deceleration of the body puts tension on the round ligament of the liver. Since the round ligment inserts at the umbilicus and terminates at Time To Develop Minutes to weeks after the injury depending on severity of the injury. Minutes to hours. A study found that 86% of these injuries heal on their own, thus the initial injury must be severe to become a life threat

blunt force

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ANTY 3400 Charteris Assignment 1

Student Name: Adam Student Number: 100312428

the falciform ligament, tension applied may result in shear forces to the inferior vena cava and hepatic artery (Rada). Excessive bleeding from either of these vessels leads to hypovolemia, shock, disseminated intravascular coagulation and systemic organ failure. Kidney can either rupture or become contused. Contused kidneys invariably self repair however, a lacerated kidney may hemorrage into the abdominal cavity as blood is lost from the renal arteries resulting in decompensating shock and death.

(Sandhyarani).

Injury to the kidney

Renl arteries bifurcate from the abdominal aorta, thus without rapid intervention death from hypovolemia and shock would result in minutes. Time to death depends on a number of factors. Bowel perforations are separated into free and contained perforations (Azer et. al). For example an upper bowel perforation may be contained by the organ adjacent to it such as the pancreas while a free bowel perforation spills its contents directly into the abdominal cavity resulting in massive septicaemia and death within hours of occurrence. It may take days or weeks for significant pH or osmotic imbalances to become life threatening (Rackley et. Al).

Perforated Bowel

Bacteria that are normally sequestered within the lumen of the gastrointestinal tract become released into the abdominal cavity causing massive immune response.

Injury to the Bladder (rupture, intraperitoneal)

Most extra peritoneal bladder injuries are associated with pelvic fractures and are thought to occur either by contact with bony fragments or shearing forces from the deforming pelvic ring (Rackley et. Al). However in Bills case if he did sustain bladder injury it is likely pressure from his lap belt on a deistended bladder caused a tear at the weakest point, along a horizontal stretch, of the bladder. In this case urine collects inside the abdominal cavity, being reabsorbed by

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ANTY 3400 Charteris Assignment 1

Student Name: Adam Student Number: 100312428

the peritoneal membrane, until the inability of the kidneys to regulate pH and metabolic waste levels in the blood causes Bill to become symptomatic (Rackley et. Al). The pancreas is relatively well protected given its high position in the peritoneum. The life threat here involves damage to the pancreas that causes the death of insulin producing cells (diabetes mellitus) or pancreatitis. A person who becomes diabetic due to pancreatic injury can experience a life threatening condition known as diabetic ketoacidosis resulting in seizures, abnormal respirations and eventually death due to CNS depression and hypoxia. If the ducts of the kidney become obstructed, the enzymes normally produced by this gland may damage the pancreas causing pain, hemorrage and/or necrosis of the pancreatic tissue (Dugdale et. Al). Large radial tears to the diaphragm will increase the work of breathing to the point where a life threatening acidosis may take hold, there is also the chance of abdominal organs herniating into the thoracic cavity (Welsford et. Al).

Injury to the Pancreas

This depends on a variety of factors. It may take a few hours for the patient to become dangerously hyperglycaemic, however, pancreatitis will take days to progress into a life threatening necrosis and destruction of the pancreas.

Diaphragmatic Rupture

Depending on the organs involved and the impact on work of breathing this may cause death in a period from a few minutes to days.

2. You are attending to Glenda, a 26 year old female who has been involved in an MVC. She was driving her car at 30 kph when she lost control on the wet roads and skidded off into a telephone pole. Her car struck the pole almost head on at 25 to 30 kph. She was wearing a seat belt but it is an older car with no airbags. Glenda is still sitting in the car complaining of pain on the left side of her chest. Her radial pulse is 122 weak and regular and her blood pressure is 114/70. Her respiratory rate is 24 deep and regular with good clear air entry bilaterally although she Page 5 of 8

ANTY 3400 Student Name: Adam Charteris Assignment 1 Student Number: 100312428 does seem to be favouring/guarding her left side. Her skin is cool, pale and diaphoretic and her pupils are 5 mm PERL briskly. On physical assessment, the chest wall is intact and while her trachea is midline, she does have significant JVD. a. List two thoracic traumatic conditions that could cause Glenda to have JVD. Two possible conditions are a myocardial contusion or cardiac tamponade. b. Explain the manner in which the above two conditions will cause Glenda to have JVD. Myocardial contusion: Heart muscle impacted by blunt force trauma leaks its intracellular contents causing electrical instability and a reduction in myocardial contractility overall since some regions are not firing synchronously with other regions. If the right ventricle is injured in this manner, the right ventricle will have increased difficulty clearing its end diastolic volume (Llyod). Blood returning from the superior and inferior vena cava will be under increased pressure as it cannot enter at an adequate flow rate causing the jugular vein in the neck to become distended.

Cardiac Tamponade: It is assumed in this case that due to injury to the heart, some region of the myocardium or blood vessel supplying it has become perforated and begun to bleed into the pericardial sac. This puts excessive pressure on the heart and inhibits its ability to fill with blood. Since the right side of the heart is more dependent on Starlings law to generate significant force of contraction, the first apparent symptom is distension of the jugular veins due to backwards failure as the right ventricle is unable to clear its end diastolic volume as mentioned above. c. Based on the information that you have, Glenda is most likely suffering from what pathology? List the confirming evidence for your conclusion. Either condition can cause reduced systolic blood pressure and elevated heart rate. However, I believe it is a myocardial contusion for a number of reasons. 1. Consider the energy involved in the crash, it requires more force to perforate the myocardium or lacerate the blood vessels supplying it than to merely bruise its component cells (Lloyd). While 25-30km/h would be painful and damaging to the human body it is more likely her heart was bruised. Another indicator of the energy delivered to the chest is the absence of broke ribs. Page 6 of 8

ANTY 3400 Charteris Assignment 1

Student Name: Adam Student Number: 100312428 2. Statistically 87% of severe chest trauma patients experience myocardial contusion while cardiac tamponade comprises less than 2% (Lloyd). 3. At some point the paramedic had to auscultate the chest in order to determine clear entry from apex to base. Muffled heart sounds would have been a noteworthy finding indicative of cardiac tamponade. A tamponade resulting from blunt force trauma would likely rapidly decompensate into cardiogenic shock even with the best ambulance response times due to severely impeded cardiac output with the tear in the myocardial tissue or hemorraging of blood vessels supplying the myocardial tissue.

Works Cited Ruptured Spleen. Mayo Clinic: Health. N.p. Nov. 2010. 17 Sep. 2011.<http://www.mayoclinic.com/health/rupturedspleen/DS00872/DSECTION=complications> Azer et. Al. Intestinal Perforation. Medscape Reference. WebMd, N.d, 17 Sep 2011.<http://emedicine.medscape.com/article/195537-overview#a0103> Dugdale et. Al. Acute pancreatitis. Pubmed Health. A.D.A.M Medical Encyclopedia, N.d, 17 Sep 2011. <http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001332/> Hannon, R. Pooler, C. and Porth, C. Porth Pathophysiology 1st Canadian ed. Philidelphia: Lippincott Williams and Wilkins, 2010. Print. Lloyd, D. Thoracic Trauma. Department of Health. State of Washington, N.d, 17 Sep 2011.<https://docs.google.com/viewer? a=v&q=cache:HWY0m0dJx88J:www.doh.wa.gov/hsqa/emstrauma/OTEP/thoracictrauma.pp t+thoracic+trauma+ppt&hl=en&gl=ca&pid=bl&srcid=ADGEEShENDbw0Yb7lt2YnmeObyQcFBFpQaHB7JZb318GiJaULF7tp0bP4MhrzVBtlSuzCjxYKEUR4OrJMEo8KXLaY7j GoLuXp4DnrIOQMBauC9AVPNqmN35khI41iG4KBj6NviPmI0&sig=AHIEtbSafz75UzdFGMPA0Hz8ue WQ8_PHjw> Malik, G. Rhabdomyolysis and Myoglobin-induced Acute Renal Failure. Saudi Journal of Kidney Diseases and Transplantation. N.p., 1998. Web. 02 Apr. 2011< http://www.sjkdt.org/article.asp?issn=13192442;year=1998;volume=9;issue=3;spage=273;epage=284;aulast=Malik>. Parham, W and Baram, D. Mehdirad, A. Hyperkalemia Revisited. Pub Med Online. N.p 2006. 02 Apr. 2011.< http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0002204/>. Rackley et. Al. Bladder Trauma Treatment & Management. Medscape Reference. WebMd, N.d, 17 Sep 2011.<http http://emedicine.medscape.com/article/441124-treatment#a1128>. Page 7 of 8

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Student Name: Adam Student Number: 100312428

Rada, J. Lacerated Liver Treatment. EHow: Health. N.p., N.d., 17 Sep. 2011.<http://www.ehow.com/way_5270008_lacerated-liver-treatment.html>. Sandhyarani, N. Lacerated Liver. Buzzle.com. N.p., N.d, 17 Sep 2011.<http://www.buzzle.com/articles/lacerated-liver.html>. Vanholder, R. Et al. Acute renal failure related to the crush syndrome: towards an era of seismonephrology. Oxford Journals: Nephrology. N.p. Apr. 2010. 02 Apr. 2011.<http://ndt.oxfordjournals.org/content/15/10/1517.full>. Welsford et. Al. Diaphragmatic Injuries in Emergency Medicine. Medscape Reference. WebMd, N.d, 17 Sep 2011.<http://emedicine.medscape.com/article/822999-overview>

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