CRITICAL THINKING INCIDENT Problem In order to be able to treat the dehydration that the patient came in with, the doctors put the patient on normal saline to raise the fluid levels. The patient ended up with fluid overload. The patient came in with dehydration and within the hospital stay acquired fluid overload, how did this happen? Background information An 85 year old female was admitted to the hospital due to a fall. The patient was diagnosed with Rhabdomylosis syncope, which is the breakdown of muscle fibers which leads to kidney damage (Rhabdomyolysis - PubMed Health). Patient has a past medical history of Wegener’s granulomatosis, which is a disorder in which blood vessels become inflamed, making it hard for blood to flow (Wegener’s granulomatosis - PubMed Health). The patient also has a past medical history of Atrial Fibrillation, glaucoma, hypothyroidism, pain in the thoracic spine, and confusion. The patient had a past cataract surgery. Upon assessment the patient had a total output of 320 mL. The patient had generalized edema and seemed to have gained weight. The patient showed signs of restlessness and change in mental status. Lab values significant to this care problem: • High WBC 11.0 (normal: 3.8-10.5 K/uL) • Low Hemoglobin 10.3 (normal: 13-17g/dL) • Low Hematocrit 31.8 (normal: 39-50 %) • Low RBC 3.63 (normal: 4.2-5.8 M/uL) • High BUN 26.0 (normal; 7-23 mg/dL) • High Creatine Kinase702 (normal: 60-400 IU/L) • High Sodium 160 (normal: 135-145 mEq/L) Medications: • Latanoprost (Xalatan): Treats ocular hypertension and open-angle glaucoma • Levothyroxine (Synthroid): Treats hypothyroidism and to prevent goiter. • Iosartan (Cozaar): it’s an Angiotensin II and is a potent vasoconstrictor • Spironolacton... ... middle of paper ... ...n assessing the patient’s lungs I did not see or hear any form of respiratory problems. The patient did not have any shortness of breath (dyspnea). The patient did not have a persistent cough or any form of wheezing. Usually in patients with heart problems they have an increase need to urinate at night, which the patient did not need to. The patient did not show any signs of chest pain which is another sign of CHF and HF. Because the patient did not show the main signs of heart problems I was able to rule out fluid overload due to heart problems. All-in-all patients may receive fluid overload for many reasons. The three main reasons why one may develop fluid overload is because of large volume of intravenous fluids, cardiac problems, or kidney failure. In my patients case the main reason as to why she developed fluid overload was because of kidney failure.
During my morning rounds I began my assessment of Mrs. M., and I noted that she had shortness of breath and she was making gurgling sounds. I immediately auscultated her lungs and noted bilateral wheezing throughout all fields, her heart was irregular and rapid and she had 2plus pitting pedal edema. I noticed she had an IV running at 125ml/hr, which I quickly stopped. The patient did not have orders for IV fluid there was only an order to KVO. I raised the head of the bed and paged respiratory to the floor.
Additionally, her radial pulse in her right arm was diminished. Her mechanical ventilator was on assist control with a tidal volume of 450ml, respiratory rate set at 12 breaths per minuet, positive end-expiratory pressure of 5, fraction of inspired oxygen at 40 percent and an end tidal carbon dioxide level of 40mmHg. She had an oral temperature of 98.5 degrees Fahrenheit, an apical heart rate of 67 beats per minute; her respiratory rate was 12 breaths per minuet, with a oxygen saturation of 98 percent and blood pressure of 127/39. Her last bowel movement was on April 2nd and is currently NPO on continuous tube feedings of Benefiber. She has a red spot on her sacrum due to
A 74 year old male with a history of COPD presents to the ED with severe difficulty breathing. His respirations are 26; chest expansion is retracting; BP is 154/76; pulse is 100 bpm; and temperature is 99 degrees F.
The patient denies any chest pain, shortness of breath, any new neurologic complaints. No nausea, no vomiting, no dysuria, no
On 1/9/18 I met Ms. Hendrick at the office of Dr. Kala, Neurologist. Ms. Hendrick reports that she had just left the lab having a repeat kidney function lab value drawn. She will find out when the values are available if she is able to have the port removed from her chest and confirm that she is not going to need more dialysis. Ms. Hendrick said she has a constant headache now. Her face still becomes numb on the right and the pain is mainly on the right side of her head. The best the pain level gets is a 5 and the worst is an 8. Now that she is limited to medications she doesn’t seem to be able to break the cycle. She reports that the Sumatriptan was not approved so she did not have that to take. Ms. Hendrick also gave me a bill that was from an MRI done ordered by Dr. Saper. I have enclosed a copy for the adjuster. All medications were reviewed; many have been stopped due to the kidney function. She no longer takes Neurontin, Lyrica, and Metformin. She will need approval by the Nephrologists before she can resume them. She does however still need the Sumatriptan injections. At this point, Dr. Kala recommends getting clearance from the Nephrologists to resume treatment with Dr. Saper. Ms. Hendrick will proceed with getting that clearance.
This is an 84-year-old Arabic patient with a significant past medical history of hypertension, hyperlipidemia, and hypothyroidism. She also has a question of osteoarthritis and gout. She came to the emergency room with pain in her right ankle and foot extending into her leg. She had difficulty in ambulating. She had no chest pain, shortness of breath or other significant symptoms. Her past medical history she has a history of hypertension, as I noted, congestive heart failure and hyperlipidemia. Her initial diagnostic testing revealed a white count of 12.4 with uric acid of 5.5, creatinine was 2.36 however her previous creatinine was abnormal at 1.43 but that was from 3 years prior. She had a CAT scan of the foot which showed an osteochondral
Physical examination is unremarkable with no evidence of leg edema, lung crepitations, heart S3 sound, or ascites. Skin turgor is normal. Laboratory studies show a normal urinalysis and CBC, with comprehensive chemistry
Critical thinking and clinical judgment are important skills that professional nurses use in every day clinical setting. In 2012, a mix method qualitative study by Dr. Jeanne Mann was done to evaluate the effectiveness of educational strategy to develop clinical judgment skills in nursing students. In this study, the population was identified as volunteered Level II baccalaureate nursing students from a Midwest nursing program. The variables identified in this article are the relation between critical thinking and clinical judgment. The title of the article clearly indicated the focus of the study and created an interest in reading the research due to nurses utilize their ability to critical think and clinical judgment in all aspect of their practice.
The purpose of this essay is to reflect and critically study an incident from a clinical setting whilst using a model of reflection. This will allow me to analyse and make sense of the incident and draw conclusions relating to personal learning outcomes. The significance of critical analysis and critical incidents will briefly be discussed followed by the process of reflection using the chosen model. The incident will then be described and analysed and the people involved introduced. (The names of the people involved have been changed to protect their privacy) and then I will examine issues raised in light of the recent literature relating to the incident. My essay will include a discussion of communication, interpersonal skills used in the incident, and finally evidence based practice. I will conclude with explaining what I have learned from the experience and how it will change my future actions.
A chest radiograph is one option which in a CHF patient will show hazy lung fields, distended vasculature, and cardiomegaly. An echocardiogram will also show heart enlargement along with ineffective ventricular contraction. Laboratory tests are one of the easiest ways to confirm it. They will show a decreased sodium and hematocrit levels, an elevated BUN and creatinine level, and an increased BNP level. Another way is a liver function test which show elevated levels that is usually linked to
Prerenal failure its common to have a decrease in urine output but not always. Fluid retention which commonly causes swelling in distal extremedies,slumberous, dyspnea, chronic fatigue and nausea. The man who arrived into the clinic had complained about almost all symptoms of acute renal failure. Intrinsic renal failure is when the direct damge causes the kidney to lose its function. Most common intrinsic renal failure is acute tubular necrosis where the small filtering
Some may think that they words acute kidney injury and chronic kidney disease mean the same thing, but that is incorrect. Kidney failure results from the kidneys not being able to eliminate metabolic waste products and water, which can also disturb all other organs of the body. Acute kidney injury (AKI) is a sudden and rapid loss of kidney function that usually occurs over hours to days due to acute tubular necrosis. Acute tubular necrosis is a process where ischemia affects parts of the kidneys and disrupts the basement membrane and the tubular epithelium. Chronic kidney disease (CKD) has a gradual onset and can take place over many years. CKD is seen in many diabetic patients due to diabetic neuropathy. AKI is a much more serious issue and should be taken very seriously.
This includes extracellular volume depletion, decreased renal blood flow, and/or injuries to the kidney cells. Acute kidney injury can be classified as pre-renal, intra-renal, or post-renal. Causes of pre-renal are due to hypovolemia, hypotension, or hypo-perfusion. Of these the most common cause of acute kidney injury is due to renal hypo-perfusion. Poor profusion can lead to vasoconstriction, hypotension, hypovolemia, hemorrhage, and inadequate cardiac output (Huether & McCance, 2012, p 754). When the body fails to restore blood volume or blood pressure, cells injury can occur and cause acute tubular necrosis or acute interstitial necrosis. Causes of intra-renal dysfunction are due to acute tubular necrosis from post-ischemic or nephrotoxic causes. Acute tubular necrosis can be caused by glomerulopathies, acute interstitial necrosis, vascular damage, malignant hypertension, coagulation defects, renal artery/vein occlusion, and bilateral acute pyelonephritis (Huether & McCance, 2012, p. 755). Post-renal injury is rare and is due to urinary tract obstruction, tumors, or neurogenic bladder that affects the kidneys bilaterally (Huether & McCance, 2012, p.
His diaphoresis subsided, but then he started coughing more vigorously with blood tinged sputum. I asked another nurse to call our lab to come and type and cross him immediately. The charge nurse, and another nurse were in the room with me. Before a phlebotomist can type and cross him, the patient started complaining of nausea, then suddenly started throwing up bright red blood with clots. I looked at his emesis bag noticed about 600 cc of blood. One of the nurses paged the doctor and explained to him what was transpiring to which he ordered 5 units of packed red blood cells and said he was on his way. The type and cross had not resulted yet and so I asked the aid to run to the lab and ask for O negative blood for this patient. Some of the nurses were perplexed and asked why O negative? I said because that’s what the doctor will say when we call him back since O negative blood can be given when you have not type and cross the patient or don’t know the patient blood type. As I was explaining myself to the nurses, the doctor walked in from the GI lab, and I said to him the type and cross had not resulted
Patient A: 45 Y/O AAF present with fatigue x2 months with some SOB with activities; no previous health