Kawasaki Syndrome (KS) is an acute, generalized systemic vasculitis of unknown etiology that often involves the coronary arteries, indicating KS as a main causative factor of acquired heart disease in American children (). KS causes more than 5,000 hospitalizations per year with 75%-85% of cases occurring in children younger than 5 years of age (). KS divided into 3 phases: acute, sub-acute, convalescent. Clinical diagnosis of KS is based on the combination of a fever > 5 days and 4 specific physical exam findings (). Fever, an essential KS diagnostic criteria, lasts for 5 days, peaks above 39°C (102°F) and is refractory to antipyretics (). Polymorphous exanthemas, persists for 10-14 days, are generalized over trunk, extremities and skin
The EB’s case study said the female patient is 50 years old with symptoms of fever, chills, congestion, three weeks of coughing, shortness of breath when walking. The study implies that the patient is now seeking medical advice due to vital signs recording and the noting of decreased breath sounds and wheezing. She denies smoking and not taking any chronic medication.
Most patients may begin with symptoms of a runny nose, cold or sinusitis that continue to persist longer than normal upper respiratory infections and fail to respond to therapeutic measures. Even though, not all patients experience all of the symptoms, the severity of the disease is different for each patient. Other symptoms can include: arthritic joint pain, blood in urine, cough (with or without presence of blood), fever, inflammation of the ear with hearing problems, inflammation of the eye with vision problems, lack of energy, loss of appetite, nasal membrane ulcerations and crusting, night sweats, numbness of limbs, pleuritis (inflammation of the lining of the lung), rash and/or skin sores, saddle-nose deformity, weakness, fatigue, and weight
starts with a tingling and weakness starting in a persons feet of legs and slowly spreading
Mrs. Jones, 78 years old, arrived in the emergency department (ED) via ambulance. She was alert and oriented, but was having episodes of lost consciousness. She was put on the cardiac monitor and her vital signs were obtained. Her cardiac rhythm was normal. Her vital signs were as follows: Temperature 97.3°F, Pulse 43, respirations 26, blood pressure 100/58 and O2 saturation of 94% on room air. Additionally, Mrs. Jones was vomiting and had 2 loose, incontinent stools. She was pale, cool to touch and diaphoretic. Auscultation of her lungs revealed expiratory wheezes.
Fever, chills, and night sweats. Fatigue and weakness. Loss of appetite and weight loss. Shortness of breath and chest pain.
This disease involves inflammation of the heart muscles or the surrounding tissues, which may be caused by bacterial, viral, or fungal infections, or by immune diseases. Those most at risk include individuals who had a congenital birth defect or previous injury to the heart, intravenous drug users, and those with an artificial heart valve.
There are a few different ways to diagnosis Rocky Mountain spotted fever. One way is through blood testing, but in some cases, a positive result does not always show in blood culturses unless the patient has a severe, late-stage infection of (RMSF). Laboratory tests can confirm the presence of antibodies to (RMSF), but these do not appear until between 7 and 10 days after the onset of symptoms. Biopsy of the rash may be performed but this test is accurate only 70 percent of the time. Typically when a doctor suspects Rocky Mountain Spotted Fever, treatment will be given to the patient even without confirmation from the lab findings (Berry, 2017).
In order to learn about Kawasaki disease we must look at its history. Kawasaki disease was simultaneously discovered around the world between 1960 and 1970. Kawasaki disease also known as Kawasaki Syndrome or Mucocutaneous lymph node Syndrome was discovered by Japanese pediatrician Tamisaku Kawasaki; hence the name Kawasaki Disease.However, KD was independently recognized as a distinct condition in the early 1970’s by pediatricians Marian Melish and Raquel Hicks at the University of Hawaii. Dr. Tamisaku Kawasaki saw his first case in the early 1960’s; subsequently, he published his first findings in Japanese in 1967 then, in 1974 he published the English version. Though it wasn’t recognized as an aggressive syndrome, it was associated with serious complications of the coronary arteries. Nevertheless,extensive research into understanding the outcome based on publications on the origin, pathophysiology, epidemiology, and treatment.
A person who has been infected by the disease may experience signs of fatigue, loss of appetite, fever, sore throat, swollen lymph nodes, and a red rash that appears blotchy. Generally the signs become present between ten and twenty-one days after the person has been exposed to and infected by the virus (Silverstein et al., 1998). This is what is known as the incubation period (Plum, J., 2001). The rash is most likely to begin on the chest, back, or the scalp, but will soon spread to the rest of the body. After a couple days of having physical evidence of the infection, the rash will s...
Other symptoms are breathing frequent and superficial, the fever and then can often present a noise very particular in the chest area, which is heard through the stethoscope. The symptom picture is completed by shortness of breath, sobs, anemia and decreased body weight.
Guillain- Barre Syndrome (GBS) is a rare, but very fatal auto- immune disease that specifically focuses on attacking the myelin sheath that surrounds the peripheral nerves in the human body. There are many different severities of this disease, but without treatment it can not only affect the entire nervous system but eventually shut down the rest of the body.
Signs and symptoms greatly depend on the initial site of infection, the causative microorganism, the underlying health history and status of the patient, the pattern of acute organ dysfunction as well as the period of time from initial onset to initiation of treatment (Angus & Van der Pol, 2013). However, classic Signs of sepsis may include but are not limited to fever, hypotension, cloudy-blood tinged urine, oliguria with sequential anurina, delirium, tachycardia, tachypnea, skin pallor, decreased temperature in extremities due to inadequate perfusion, increased lactate as well as altered blood glucose levels and blood cell
is characterized by “deterioration in the level of consciousness, with lethargy, decrease in arousal and headache. The timing of the development of cerebral edema is variable, within most cases occurring 4 to 12 hours after starting treatment. Several case reports showed the presence of cerebral edema before the initiation of therapy. A method of clinical diagnosis based on bedside evaluation of a neurological state in DKA have been developed” (Pandey).
The patient is a 30 year old male with an active bacterial infection on his right leg attacking his Integumentary system. The patient is from Tanzania, Africa but came back to work in a factory that produces plastic. If he has Cellulitis, it can get bad enough to travel to other organs like the Liver and Kidney and cause failure. If this happens, Edema can form, usually on one half of the body; this is the Urinary system being attacked. The main system being attacked is the Lymphatic system because Cellulitis attacks the lymphatic draining system. For Cellulitis to travel to organs, it had to go through the blood, so the cardiovascular system is also in effect.
MEDICAL DIAGNOSIS: Empyema, Hemoptysis, Necrotizing pneumonia, Aspergillosis (Aspergillus fumigatus) cachexia secondary to malnutrition/infection, hypothyroidism, Diabetes Type II melitius , and...