My Ssec Capstone Project Physical Examination

Physical Examination

Physical Examination:
When we started our assessment, we did not find any signs of trauma on the patient. The floor was carpeted and it seems that she had a low impact fall, therefor we did not take C-spine precautions.
M.P. was responsive to pain, her airway was open and was breathing effectively. She had a weak, rapid, regular radial pulse. No central or peripheral cyanosis was noted.
On the rapid body survey, we found no abrasions, masses or contusions either on her head or neck. No jugular vein distention, trachea deviation or accessory muscle use was noted. .Her eye sclera was slightly yellow. Her chest had equal air expansion and we did not find any adventitious sounds on auscultation. Her abdomen was severely distended and firm. There was no Cullen sign (ecchymosis or bruising around her umbilicus) or Grey Turner’s sign (ecchymosis on her flanks). No crepitus or deformities were noted on her hips. We found bilateral pedal edema on her lower legs. Her arms had several skin tears, some of which looked a couple of days old while others looked fresh and were still bleeding. It did not look like any of the tears were caused by the fall, since there was nothing around her body that she could have hit it with, causing those scratch like tears. When we applied a trap squeeze, M.P.’s hands started flapping with the characteristic tremors consistent with asterixis movements or “liver flap”. These are the repetitive clonic movements of the wrist when they are hyperextended, a classic sign of liver failure (R Agarwal & R Baid., 2016) . Her skin was jaundiced, warm and dry. We also performed a glucose test with a glucometer which showed normal levels of glucose in her blood.
M.P.’s initial Vital Signs are as follows:
LOC: Responsive to Pain
GCS: 2, 3, 4
Pulse: 95 weak, regular radial
Blood Pressure: 88/50 mmHg
Respirations: 24 shallow and effective
Skin: Jaundiced, warm and dry
Pupils: Equal and reactive, 3 mm.
SPO2: 97%
BGL: 6.9 mmols
Temperature: 36.5oC

Past Medical History:
When we started inquiring about M.P.’s past medical history, the daughter stated her mom contracted Hepatitis C approximately 15 years ago by a blood transfusion and was diagnosed a couple of years ago with liver cirrhosis. She also states that her mother was in the hospital last week to drain some of the fluid that has been accumulating in her abdomen. She states that even though M.P.’s illness has been progressively getting worse and she has been showing signs of mental confusion she has never lost consciousness like this.
Medications: Furosemide 40 mg. OD; Syntroid 75 mg. OD; Quetapine 25 mg. OD; Mirtazapine 15 mg. OD; Spironolactone 100 mg. OD.
Allergies: Daughter denies her mother having any allergies.
Functional Enquiry:
Since M.P. was unable to answer any questions, her daughter had to help us with the functional enquiry. She denied any history of seizure disorders, strokes or transient ischemic attacks. She states that her mother suffers severe headaches very often and has been getting pretty confused lately. She denies any history of heart problems, high blood pressure, hyperlipidemia or diabetes. She states her mom has had hypothyroidism since her early twenties and takes medication for it. She denies her mother having asthma or COPD. She states M.P.’s abdomen has been filling up with fluid for approximately a year and now it has to be drained weekly at the hospital. She states she has been getting a lot more jaundiced in the past few weeks and has been also complaining of severe skin itchiness, which can be so severe at times that it keeps her awake at night. She also says her mother’s sleep pattern has changed and she sleeps very little at night while sleeping for long periods of time during the day. She states her mother’s skin has been tearing very easily when she scratches herself. She says her mom is constantly bleeding from the tears and she does not allow her kids to touch grandma anymore since she is scared they may contract Hepatitis C. She also states she is unable to keep on caring for her mom by herself due to her job and having young children. She says she is in desperate need of help to care for her mom.

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Differential Diagnosis 1: Hypovolemia due to severe ascites
M.P.’s severely distended abdomen suggests she is suffering from ascites.

Ascites is the abnormal accumulation of fluid in the abdominal cavity and it is a common complication of cirrhosis. Approximately 50% of patients with cirrhosis develop this condition. Ascites occurs due to portal vein hypertension.

In a cirrhotic liver, cells are unable to repair themselves. When the liver cells die, fibrotic scar tissue is formed impeding proper blood flow. In a healthy liver, blood enters it through the portal vein and when the liver tissue is damaged and scarred, blood flow is obstructed causing stress on the portal vein, triggering high blood pressure or hypertension in the liver.

As portal hypertension develops, splanchnic (visceral) arterial vasodilatation occurs and it can be so pronounced that the arterial blood volume decreases dramatically causing systemic blood pressure to fall. Researchers think that it is the combination of portal hypertension and splanchnic arterial vasodilatation that alter intestinal capillary pressure and permeability, which cause plasma to leak out of the blood vessels causing ascites. Lymph formation that exceeds lymph return can also occur, contributing to the fluid accumulation in the peritoneal cavity. In severe cases, ascites can lead to hypovolemia due to extreme intravascular fluid volume loss, which in turn can cause severe hypotension and ultimately shock. (Guines ; Quintero, 1957)
Even though this differential could explain some of M.P.’s signs and symptoms, it is unlikely to be the sole cause of her altered level of consciousness, since her Mean Arterial Pressure was still over 60 mmHg and therefore her brain should have being still actively perfused (Rao et all, 2013).

Differential Diagnosis 2: Hemorrhagic Shock due to Gastrointestinal Bleeding
Gastrointestinal bleeding is a life threatening complication of portal hypertension. Portal hypertension increases venous pressure and can cause bulging veins or varices in the esophagus, ileum, colon and rectum. Acute bleeding from esophageal varices is often a dramatic event since patients vomit bright red blood (hematemesis) but in some cases hematochezia (blood in the stools) and melena (dark, tarry stools containing digested blood) might be the only symptoms. Depending on the amount of lost blood, patients might be hemodynamic unstable and present in hemorrhagic shock (Biecker, 2013). Liver disease also affects the hematological system responsible for bleeding and clotting. Platelets, fibrinogen and other clotting factors are affected when the liver is not working properly, making it very difficult for the body to be able to stop major bleedings due to its impaired clotting ability (coagulopathy).
It was impossible to identify abdominal distention due to gastric bleeding on M.P. since her abdomen was already very distended due to the ascites. There were no visible signs of hematemesis around the patient, and her daughter did not know if her mother had been having hematochezia or melena so this differential diagnosis remains as a possibility.

Differential Diagnosis 3: Sepsis
Sepsis is a life-threatening condition that arises when the body’s response to infection causes injury to its own tissues and organs Patients with decompensated cirrhosis are much more prone to bacterial infections than the general population. The reason or mechanism for the increased susceptibility to infections is still unclear, but it has been suggested that patients with cirrhosis have depressed neutrophil phagocytic and intracellular killing capabilities of Staphylococcus aureus and Escherichia coli among other types of bacteria. Another theory is that in cirrhosis, sepsis is caused by an imbalanced cytokine response (cytokines are proteins released during an inflammatory or immune response), which causes an excessive proinflammatory response and seems to worsen the liver function contributing to the development of system failure such as shock, renal failure, ARDS (Acute Respiratory Distress Syndrome), coagulopathy and hepatic encephalopathy.

The most common infection in patients with cirrhosis is spontaneous bacterial peritonitis. Studies have discovered that bacteria passes through the intestinal mucosa into the peritoneal cavity due to increased intestinal permeability causing inflammation and infection of the peritoneum which in turn can lead to sepsis.

According to the BC Sepsis Network created in June, 2012, M.P.’s signs and symptoms definitely met the criteria for sepsis or Systemic Inflammatory Response Syndrome (SIRS). She was also hypotensive and one of the symptoms of sepsis is hypotension.
Hypotension in sepsis is caused not by fluid loss but rather vasodilation. Following the BC Sepsis Network guidelines we immediately initiated an IV and started administering fluids to her. It is impossible for us in the pre-hospital setting to know if this was the cause for M.P.’s altered level of consciousness, but we definitely were able to start treating her hypotension with fluids and see if this could correct it.

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