Discuss about the Elderly Fall Patients Triaged To The Trauma Bay.
Gastroenteritis is defined as inflammation of the gastrointestinal tract comprising the stomach and small gut due to infection with bacterial, viral or other microbial, usually presenting as diarrhea, vomiting and abdominal pain (Walker & Colledge, 2013).
Gastritis is the inflammation of the stomach’s mucosal lining (Walker & Colledge, 2013). It is either chronic or acute and can be infectious or noninfectious. Most commonly caused by bacterium Helicobacter pylori.
Skin turgor in relation to gastroenteritis
The patient presented with a poor skin turgor due to the disease process. Reduced skin turgor in gastroenteritis is due to dehydration that follows diarrhea and vomiting, the cardinal presentations of gastroenteritis (Smeltzer et al., 2008). In dehydration, the skin elasticity is reduced as the cells lose water leading to a poor skin turgor.
Blood pressure in relation to the scenario
The patient's blood pressure is low due to hypovolemia, a relative reduction in blood volume due to unreplaced fluid losses in vomiting and diarrhea. Since blood pressure is a product of cardiac output and total peripheral resistance, a reduction in blood volume will reduce preload, which will reduce cardiac output thus lowering the blood pressure (Smeltzer et al., 2008).
Signs and symptoms of gastroenteritis
The most common presenting symptoms of gastroenteritis are vomiting, diarrhea and abdominal pain. The relevant signs of gastroenteritis include fever and abdominal pain (Walker & Colledge, 2013).
Pathophysiology of multiple sclerosis
Multiple sclerosis is a disease of the central nervous system demyelination. This is due to autoimmunity with chronic inflammation leading to loss of myelin on nerve fibers. The chronic inflammation leading to loss of myelinated nerve fibers leads to loss of function in those affected areas and disability that spans many years. The immune process leads to the formation of plaques, hence the term sclerosis. The immune cells involved include lymphocytes, monocytes, and macrophages which infiltrate nerve fibers and strip off myelin with associated axonal injury (Korn, 2008).
Signs and symptoms of multiple sclerosis
Symptoms are varied according to the pathologic process and include sensory loss, visual loss, weakness, change in bladder or bowel function, cognitive changes and disability just to mention a few (Korn, 2008).
Rhabdomyolysis is defined as muscle breakdown due to direct or indirect injury with accompanied release of breakdown products into the bloodstream (Graham et al, 2004).
Medication causing rhabdomyolysis
Anti-cholesterol medication that has effects on muscle and causes rhabdomyolysis is the class of drugs called statins (Graham et al, 2004). They include atorvastatin, rosuvastatin, simvastatin, and pravastatin. The patient is educated about this medication, its effects on reducing cholesterol levels and the potential side effect of rhabdomyolysis. They are instructed to discontinue the medication and seek immediate medical assistance if they experience muscle pain while on the medication.
The medical definition of black stools is melena and is an implication of lower gastrointestinal bleeding (Zhu et al, 2018). The stools are black and not the red color of blood due to a possible bleeding source higher up the gut thus allowing the blood enough time to break down and decompose.
Emesis and hematemesis
Emesis is the involuntary expulsion of gastric contents and is the medical term denoting vomiting. When the product being vomited is blood, this is termed hematemesis (Laine et al, 2018).
Pathophysiology of hematemesis and melena.
The patient admitted with both hematemesis and melena could be due to an upper gastrointestinal tract bleeding source probably before the stomach (Laine et al, 2018). Hematemesis is directly from the bleeding source as the patient vomits fresh red blood. However, the patient swallows some of the blood and this blood is propagated down into the lower gastrointestinal tract, having enough time for breakdown and decomposition, leading to `the expulsion of melena stool.
Yellowing of sclera and skin.
Yellowing of the sclera and the skin is termed jaundice and usually involves the liver which is the main organ involved in the production of bile, the main excretory route for bilirubin (Walker & Colledge, 2013).
Pathophysiology of jaundice
An example of a disease process that might cause jaundice is viral hepatitis. In viral hepatitis, the hepatocytes are infected by the virus and damaged as a consequence of the adaptive immune response to viral elements (Walker & Colledge, 2013). The hepatocytes are destroyed leading to impaired conjugation of bilirubin and secretion of bile into the intrahepatic duct system. Bilirubin accumulates in the blood and is deposited in tissues especially the skin giving the characteristic appearance of yellowing of the skin and sclera (Walker & Colledge, 2013).
Pruritus is defined as the unpleasant sensation that provokes the desire to scratch with the presentation of itching of the skin.
A hernia is an abnormal protrusion of a tissue from its normal location into another compartment through a wall that normally contains it.in the case of a hiatal hernia, the upper part of the stomach herniates through the diaphragm hiatus into the chest compartment (Kahrilas, Kim, & Pandolfino, 2008). It may present with symptoms of chest pain, nausea, and vomiting but most may be asymptomatic.
GORD stands for gastro-oesophageal reflux disease and is the backflow of gastric contents into the oesophagus due to incompetent lower oesophageal sphincters (Walker & Colledge, 2013).
Nursing care plan for Michael.
- The first patient issue identified is diarrhea which is the passage of loose, unformed stool. It is the commonest presentation in gastroenteritis and could be as a result of bacterial, viral or parasitic infection.
The desired goal is that the patient will pass formed stool for more than three times in a day.
The nursing interventions include administering antidiarrheal medication as prescribed and teaching the client about the importance of handwashing after each bowel movement.
- The second patient issue identified is fluid volume deficit possibly related to diarrhea, vomiting and inadequate intake and evidenced by poor skin turgor. The desired outcomes are normovolemia by return of blood pressure to normal range and return of skin turgor.
The nursing interventions venous access with the administration of intravenous fluids, monitoring losses in vomitus and urine and adjusting the fluid input appropriately. Medication administered as ordered. Including antiemetics and oral rehydration salts.
- The other issue is GORD as evidenced by the patient complains. The goal is to reduce pain and discomfort by administering anti-acids medication as prescribed and monitoring for any changes.
It is a chronic joint disease due to degenerative changes in the articular surfaces of bone also termed “wear and tear disease”. Factors present that could have contributed to the development of osteoarthritis in Carol Brady include her age and gender (Bijlsma, Berenbaum, & Lafeber, 2011). Since it is a degenerative disease, incidence increases with age. The patient is aged 78 years old hence falls into this category. This is due to wear and tear due to repeated articular surfaces compounded by the age-related weakening of cartilage. After 56 years of age, the incidence is also noted to be higher in females although reasons for this are poorly understood (Bijlsma, Berenbaum, & Lafeber, 2011).
Education in osteoarthritis
The patient should be made aware that there is no specific treatment to halt joint degeneration or reverse the damage already done and that goals of therapy will include pain reduction, reducing inflammation and maintaining joint function. The patient is taught some conservative measures to help alleviate symptoms including rest, diet control, weight reduction and exercise (Bijlsma, Berenbaum, & Lafeber, 2011).
Pathophysiology of Parkinson’s disease and falls
Parkinson’s disease is a chronic neurodegenerative disease due to the progressive loss of dopaminergic neurons (Jankovic, 2008). The process occurs over time hence incidence is highest in the elderly although the exact mechanism of dopamine loss is unclear. The loss of dopaminergic neurons leads to defects in the neural centers dependent on dopamine as a neurotransmitter especially the basal ganglia which has cortical connections to mediate movement (Jankovic, 2008). This leads to the typical presentation of tremors, bradykinesia, rigidity and postural instability. This is the main reason these patients are predisposed to falls.
Parkinson’s disease symptoms.
Symptoms can be termed motor or non-motor. Motor symptoms include bradykinesia, akinesia, tremors, rigidity and postural instability. Others include hypomimia, dysarthria, dysgraphia, festination, freezing, and dystonia. Non-motor symptoms include cognitive impairment, sleep disturbance, hallucinations, autonomic dysfunction and sensory deficits for example anosmia (Jankovic, 2008).
Apart from vital signs, other observations in this patient should include a Glasgow coma scale, urine output, fluid and electrolyte input, and pain rating. Since this is a fracture patient, blood loss and shock are valid concerns leading to the initiation of fluid therapy through a wide bore cannula as signs of deteriorating fluid status are noted for example the blood pressure and pulse rate. However, fluid replacement should be accompanied by appropriate monitoring of output using a Foley catheter to measure outputs.
Falls in an elderly patient tend to be associated with unrecognized head trauma hence serial monitoring of the Glasgow coma scale to note any neurological deficits could be of help to rule out serious brain injury especially subdural hematoma.
Pain is another important aspect of management in these patients and a verbal pain assessment is another observation that is mandated to aid analgesia.
Nausea and vomiting.
Falls in elderly patients are usually associated with acute head injury (Evans et al, 2015). The trauma from the fall could have ruptured a blood vessel that slowly bled leading to either a subdural, epidural or intracerebral hemorrhage. These pathologies will present with neurological deficits of note being signs of increased intracranial pressure as the accumulated blood causes a mass effect in the otherwise volume restricted cranium.
Signs of increased intracranial pressure include a headache, nausea, and vomiting which the patient has experienced and this could explain the presentation (Smeltzer et al, 2008).
Nursing care plan for Carol
- The patient problem identified was impaired physical mobility related to fracture radius or limb immobilization. The desired outcome is regaining of purposeful movement and maintain function. The nursing interventions in this regard include assist with self-care activities including bathing and encourage early ambulation.
- The second issue identified was acute head injury as evidenced by signs of increased intracranial pressure. The goal of the plan is to decrease the intracranial pressure seen in improving symptoms. The interventions include administer oxygen and hyperventilate the patient. Also, administer medication including mannitol as prescribed.
- The third issue was acute pain related to soft tissue injury and osteoarthritis. Desired outcomes include patient verbalizing pain relief. The interventions include maintain immobilization of affected part and administer medication as indicated including narcotics, NSAIDS, and
Allied health worker inclusion
In regard to Carol’s allergy to dairy foods and poor appetite, I would involve a nutritionist in the management of the patient as their nutritional needs need to be met if proper healing and treatment id to be achieved.
The role of a nutritionist in the management of the patient would be to provide advice and individualized nutritional charts based on the available best diet with the patient condition and needs in mind. The nutritionist should be able to find alternative foods that offer good nutritional value without causing harm or allergy to this patient.
Pathophysiology of decompression sickness
Decompression sickness is a condition due to sudden pressure changes from deep sea diving (Bühlmann, 2013). The body is affected in predictable ways by pressure change. Water is incompressible; however, gases are compressible. In the body, these gases include those in hollow organs and dissolved in blood. A reduction in pressure during ascent releases dissolved gases especially nitrogen, forming gas bubbles in the body. The bubbles have varying effects on body systems including emboli, blocking circulation leading to ischemia, activation of coagulation, and mechanical effects on vessel walls (Bühlmann, 2013).
Signs and symptoms of decompression
Signs and symptoms affect nearly all body systems. They include confusion, altered mental status, fatigue, joint pain and weakness, visual symptoms, dyspnoea, hemoptysis, chest pain, abdominal pain, paraesthesia, paralysis and headache (Bühlmann, 2013).
Treatment of decompression sickness
Treatment options involve immediate stabilization by administering 100% oxygen, intubation if necessary and venous access for administration of fluids. Cardiopulmonary resuscitation is done as required and needle aspiration if pneumothorax is suspected. After the initial stabilization, the patient should be transferred to the nearest facility that offers hyperbaric oxygen therapy for definitive treatment (Bühlmann, 2013).
Recommended time between diving and flying
Flying after diving workshops produced the following guidelines:
- When diving within no-decompression limits, for example, recreational diving, it is recommended that for single dives a minimum of 12 hours and 18 hours for multiple dives be observed before flying (Dive the world, 2003).
- When diving that requires decompression stops it is recommended that the diver take a pre-flight interval of greater than 18 hours (Dive the world, 2003).
These, however, apply to those without symptoms of decompression and need only be applied in flights that ascend over 600 meters of altitude.
Flying into high altitude areas
The conditions at high altitude which are due to low oxygen saturation have impacts on body physiology (Gudmundsson & Gudbjartsson, 2009). Travel to these areas without proper acclimatization could thus lead to these effects. Those traveling should, therefore, familiarize themselves with standard acclimatization protocols and symptoms of altitude-related illnesses. The trip should allow adequate time for adjustment and acclimatization. Maintaining hydration increases the body’s ability to acclimatize. For those with pre-existing conditions, medications should be in good supply and within reach. Some medications, for example, acetazolamide and dexamethasone help in acclimatization hence can be taken as an alternative (Gudmundsson & Gudbjartsson, 2009). Traveling in groups is another recommendation as help is within reach and others can easily recognize the symptoms of altitude sickness. Risk factors include pre-existing medical conditions and non-optimal physical fitness (Gudmundsson & Gudbjartsson, 2009).
Symptoms to look out for in high altitude area.
Symptoms of altitude-related disease include headache, abdominal pain, fatigue, dizziness, sleep disturbance, dyspnoea, exercise intolerance and productive cough. Others include difficulty walking, severe lethargy, and change in mental status (Gudmundsson & Gudbjartsson, 2009).
Differences in presentation between heat stroke and heat exhaustion
Heat stroke is a progression of heat exhaustion and is more severe requiring immediate medical attention. Heat exhaustion results from activities that overwhelm the bodies cooling mechanisms and present as profuse sweating, weakness, nausea, vomiting, headache, dizziness and muscle cramps. When the cooling mechanisms fail, the patient progresses to heat stroke which is characterized by altered mental status with confusion, severe lethargy, seizures, elevated body temperature and cessation of sweating (Epstein & Roberts, 2011).
Hypothermia is low body temperature due to rapid loss of heat that overwhelms the body’s capacity to balance. The signs and symptoms include excessive shivering, slurred speech, and fatigue (Brown, Brugger, Boyd, & Paal, 2012).
Removing impaled objects in penetrating injury can cause more harm as it can compromise further the vascular integrity of the site and cause more bleeding. The aid should have applied firm pressure and applied a dressing around the wound to control the bleeding taking care not to push the stick further in. this should be done while emergency help is sought for proper care.
Benzodiazepine toxicity presents as dizziness, confusion, blurred vision, anxiety, agitation and sometimes unresponsiveness. Signs include hallucinations, slurred speech, coma, altered mental status, amnesia, agitation, hypotonia and weakness (Veiraiah et al, 2011).
The Australian hotline in case of poisoning or overdose is 131126.
Head injury symptoms
Signs to look for in suspected head injury include worsening headache, loss of consciousness, nausea, vomiting, seizures, disorientation, memory loss and otorrhea (Walker & Colledge, 2013).
It is an injury caused by a blunt object or collision with a blunt surface that exerts mechanical force to the body (Walker & Colledge, 2013).
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