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REASON
CHIEF COMPLAINT: Hypertensive nephropathy.
BLANKLINE
Mr. Porter is a 54-year-old gentleman with severe vascular disease who was probable hypertensive nephropathy. His creatinine was 1.9 in 2009, 2.1 in 2011, 2.0 in 2012, 2.4 in 2013, and in 12/2016 it was still 2.4. Unfortunately, in association with a foot wound and vancomycin and Zosyn infusion that he has had this month his creatinine is now up to 3.7. Other labs: Past renal ultrasound unremarkable. Microalbumin to creatinine ratio elevated at 440. No urine protein on dipstick. ANA negative. A 06/2015 ultrasound negative. Sodium lower at 129, potassium 3.6, bicarb 16, glucose 289, BUN 45, creatinine 3.7, anion gap 7, so this is all renal disease. Calcium 7.4, hemoglobin
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Peripheral vascular disease, associated foot wounds, status post angioplasties and surgeries in the past.
PHYSICAL EXAMINATION
Temp 94, blood pressure 147/83. An ill-appearing gentleman lying in bed, getting an infusion. Heart: Regular rate and rhythm. Lungs: Clear. Extremities: No edema.
ASSESSMENT AND PLAN
1. Acute on chronic renal failure, hypertension and vascular disease are the most likely cause of his chronic kidney disease due to the long duration of diabetes and lack of proteinuria. Baseline creatinine can be summarized as being around 2.5 from 2014 to 12/2016. It is now 3.7, due to his wound infection and possibly vancomycin toxicity.
2. Hypertension. Adequate control given illness. We do not want his pressure to run too low.
3. Hyponatremia. Mild, would avoid excess free water and continue to monitor, if it drops lower will need to fluid restrict.
4. Acidosis, due to the acute renal failure. Non gap.
SUMMARY
1. I would suggest check the vancomycin trough that is pending, it is almost certainly going to be high and the vancomycin will need to be held. The cultures seem to indicate that this may be more of a gram-negative problem, in which case the vancomycin can be stopped. I would try to minimize the vancomycin if the creatinine continues to rise, perhaps changing to linezolid or daptomycin would be worth
There are two types of glomerulonephritis—acute renal failure (ARF) and chronic kidney disease (CKD). The ACF form generally develops suddenly as a result of an infection or illness, such as, group A streptococci bacteria, hepatitis, or in diseases such as lupus or HIV (Mathias, 2013). This type may require dialysis to replace renal function while it lasts, however, kidney function usually returns after the primary illness is treated. Many acute patients will not have any other complications as no permanent damage is done. Whereas CKD is found in a person that has had glomerulonephritis for months to years in some cases and may be asymptomatic until the kidney has become irreversibly damaged. ARF can evolve to become chronic if the glomeruli do not respond to
The kidneys play a major role in the blood composition and volume , the excretion of metabolic wastes in the urine, the control the acid/base balance in the body and the hormone production for maintaining hemostasis. The damages to the GBM in the glomeruli alter filtration process that allows the protein and red blood cells to leak into the urine. Loss of protein like albumin in the urine results in a decrease of their level into the blood stream. Consequently, this patient’s blood reveals a decreased albumin (Alb) value of 2.9 g/dL, decreased serum total protein value of 5 .0 g/dL and in the urine presents of the protein and the RBCs. Impaired filtering capacity result in inability of kidneys to excrete excretory products like electrolytes and metabolic waste products that will then accumulate in the blood. Furthermore, inability of distal convoluted tubules to excrete sufficient quantities of potassium, sodium, magnesium (Mg), chloride (Cl), urea, creatinine (Cr), alkaline phosphatase (Alk Phos), and phosphate (PO4) results in their elevation in the blood. His laboratory values reveal an increased of sodium value of 149 meq/L, an increase of potassium value of 5.4meq/L, increased chloride value of 116 meq/L, increased blood urea nitrogen (BUN) serum of 143 mg/dL, and increased creatinine serum of 7.14 mg/dL. The other abnormal blood tests associated with a loss of kidneys’ filtration property identify in this patient are related to an increase of alkaline phosphatase value of 178 IU/L, increased magnesium value of 3.8mgdL, and increased phosphate (PO4) value of 5.9 mg/dL .
Client Profile: Lane Bronson is a 55 year old male with a history of angina, hypertension, Type 2 diabetes, COPD, and sleep apnea. He comes to the physican’s office complaining of worsening shortness of breath. His skin tone is grey, and his angina is worsening. Previously stable, he now does not get relief from rest or nitroglycerin. The physician called 911 and had Mr. Bronson directly admitted to the hospital.
An electrocardiogram (ECG) is one of the primary assessments concluded on patients who are believed to be suffering from cardiac complications. It involves a series of leads attached to the patient which measure the electrical activity of the heart and can be used to detect abnormalities in the heart function. The ECG is virtually always permanently abnormal after an acute myocardial infarction (Julian, Cowan & Mclenachan, 2005). Julies ECG showed an ST segment elevation which is the earliest indication that a myocardial infarction had in fact taken place. The Resuscitation Council (2006) recommends that clinical staff use a systematic approach when assessing and treating an acutely ill patient. Therefore the ABCDE framework would be used to assess Julie. This stands for airways, breathing, circulation, disability and elimination. On admission to A&E staff introduced themselves to Julie and asked her a series of questions about what had happened to which she responded. As she was able to communicate effectively this indicates that her airways are patent. Julie looked extremely pale and short of breath and frequently complained about a feeling of heaviness which radiated from her chest to her left arm. The nurses sat Julie in an upright in order to assess her breathing. The rate of respiration will vary with age and gender. For a healthy adult, respiratory rate of 12-18 breaths per minute is considered to be normal (Blows, 2001). High rates, and especially increasing rates, are markers of illness and a warning that the patient may suddenly deteriorate. Julie’s respiratory rates were recorded to be 21 breaths per minute and regular which can be described as tachypnoea. Julies chest wall appeared to expand equally and symmetrical on each side with each breath taken. Julies SP02 levels which are an estimation of oxygen
J.P., a 58 year old female, presents to the Emergency Room on March 18th. She has a past medical history of cervical cancer, atheroembolism of the left lower extremity, fistula of the vagina, peripheral vascular disease, neuropathy, glaucoma, GERD, depression, hypertension, chronic kidney disease, and sickle cell anemia. She complains of right lower extremity pain accompanied by fatigue, a decreased appetite, increased work of breathing, burning urination, and decreased urine output for three days. Upon admission, a complete physical assessment was performed along with a blood and metabolic panel. The assessment revealed many positive and negative findings.
The patient is a 55-year-old man admitted to the hospital for dehydration secondary to vomiting. The physical examination of the patient revealed dry mucous membranes and vital signs as follows: Pulse 110, blood pressure 100/60, and respirations of 20.
The physician’s notes indicated a temperature of 98 degrees F, an elevated heart rate and respiratory rate, and low blood pressure. When the amount of oxygen available for the heart is low, it puts pressure on the heart and causes the heart rates to increase. To compensate for the low amount of oxygen the respiratory rate also increases to enable the intake of more oxygen that is be available for the body.
United States Renal Data System (USRDS). (2008). Annual data report: Incidence and prevalence. Retrieved July 8, 2009, from http://www.usrds.org/2008/pdf/V2-02-2008.pdf
D. standing near her room, breathing sharply. While asked what has just happened, she answered, ‘I feel dizzy and can faint!’ Mrs. D. then explained that she rose up from her chair in the television room and felt lightheaded. I decided to bring her to the room hoping she would feel less dizziness if she could sit. After consultation with my mentor and third year unit nursing student, I decided to perform measurement of her vital signs. Since only electronic sphygmomanometer was available for me that time, I had to use it for my procedure. Gladly, I discovered that I have already used such equipment in my previous nursing practice. Using the standard sized calf, I found that her blood pressure was 135/85, respirations were 16, and her pulse was 96 beats per minute (bpm). However, I decided to recheck the pulse manually, founding that it was irregular (78 bpm). The patient stated that she felt better after rest. Immediately after the incident I made a decision to explore carefully the medical chart of Mrs. D., along with her nursing care plan. That helped me to discover multiple medical diagnoses influencing her
Cardiovascular System: He does not experience any chest pain or palpitation. He does not have dyspnea or leg swelling.
According to the results of the tests, the patient syndrome is caused by either of the two; minimal change and focal segmental glomerulosclerosis. The pathophysiologies of the disease are primary glomerular defect and circulating permeability factor and inhibitors. The primary glomerular defect of nephrotic syndrome leads to leakage of high molecular mass proteins that’s equivalent to the size of albumin of approximately 66 kD, with haemostatic proteins of a similar size also being excreted pathologically in the urine (Eddy AA and Symons JM, 2003). Due to these excretion; prominent loss of important coagulation regulatory proteins such as antithrombin and protein S.
If the patient has a urinary catheter, and most ICU patients do, he or she may not have any reportable symptoms. Therefore, good assessment of urinary elimination, done in relation to a patient’s signs, symptoms, urine amount, intake and output, and lab values, is important. The lab values are discussed in Chapter 5. Acute and chronic renal failure can cause numerous systemic symptoms and altered homeostasis ( Collins, 2011). See Table 3-10 for abnormal urinary elimination.
This reflection of vital signs will go into discussion about the strengths and weaknesses of each vital sign and the importance of each of them. Vital signs should be assessed many different times such as on admission to a health care facility, before and after something substantial has happened to the patient such as surgery and so forth (ref inter). I learned to assess blood pressure (BP), pulse (P), temperature (T) and respiration (R) and I will reflect and discuss which aspects were more difficult and ways to improve on them. While pulse, respiration and temperature were fairly easy to become skilled at, it was blood pressure which was a bit more difficult to understand.
Rationale: Early signs of dehydration include thirst and cessation of perspiration, muscle cramps, nausea and vomiting, lightheadedness, and orthostatic hypotension. Ackley and Ladwig p. 345
The patient has high temperature-sign of fever, a very fast pulse rate (tachycardia), and chest wheezing when listened to using a stethoscope (Harries, Maher, & Graham, 2004, p.