Zev - Laboratory and Diagnostic Evaluation

8/7/2019 Zev - Laboratory and Diagnostic Evaluation

1/6


2/6

2/25/11 Diff. Count: Monocytes 01 2 9% Low low monocyte count

is not generally seen as a

clinical problem

2/23/11 Sodium 148 135 145 mmol/L High high sodium level is

caused by high FBS leveland administration of

corticosteroids

2/23/11 Potassium 3.5 3.6 5.5 mmol/L Low hypokalemia is

mostly seen inclients

undergoing insulin therapy

2/26/11 Magnesium 1.2 0.8 1.0 mmol/L High hypermagnesemia

may be caused by the

breakdown or destruction

of blood cells

2/26/11 Ionized Calcium 1.41 1.12 1.32 mmol/L High hypercalcemiamay

be caused by

administration of diuretics

2/15/11 Coagulation Studies

PT

CTAct %

Ratio

INR

Patient

14.3

14.9107.2

0.95

1.0

29.9

10-12 secs

1-2

Prolonged clotting time

may be caused by vitamin K

deficiencies leading toprolonged bleeding

2/25 PT

CT

Act %Ratio

INR

Patient

15.5

14.9

93.51.04

1.05

30.2

10-12 secs

1-2

Prolonged clotting time

may be caused by vitamin K

deficiencies leading toprolonged bleeding

02-15-11

2D ECHO

Interpretation:

Concentric left ventricular hypertrophy with adequate wall motion and contractility with Doppler evidence of relaxation abnormally


3/6

Dilated left atrium with left atrium volume of 27ml/m2

Dilated 2 atherosclerotic aortic root

Aortic sclerosis with no restrictions of motion

Trivial tricuspid regurgitation RA, RV,PA dimensions

>there is an enlargement of the left ventricle of the heart, with the capability of generating greater forces and higher pressures,

while the thickened walls maintain normal wall stress, making it stiff which can impair filling and lead to diastolic dysfunction.

>there is also a build up of fatty materials within the walls of 2 aortic roots, causing narrowing of the aortic roots.

> tricuspid regurgitations may be caused also by disorders involving the left side of the heart.

02-15-11

Electrocardiogram

Interpretation: normal sinus rhythm

Intraventricular conduction defect

Left ventricular hypertrophy by voltage with strain pattern

Non-specific ST T wave changes

02-21-11

Normal sinus rhythm

Possible old inferior wall infarct

Non-specific ST T wave changes

> Intraventricular conduction defect may be caused an inflammatory disease.

>there is an enlargement of the left ventricle of the heart


4/6

> Non-specific ST T wave changes may be caused by electrolyte imbalances or cerebrovascular accidents

02-16-11

Chest AP X-ray

Film taken in poor inspiration.

There is accentuation of the pulmonary vascularity.

The heart is widened.

Aorta is faintly calcified.

There is bilateral hilar fullness.

Diaphragm and costophrenic sulci are intact.

Impression: Widened cardiac silhouette with signs of bilateral pulmonary congestion

Atherosclerosis, thoracic aorta

>there is a build up of fatty materials in the thoracic aorta

> there is fullness in the shadow in the both sides of the chest.

> There is a recess between the ribs and the lateral-most portion of the diaphragm, partially occupied by the most caudal part of the

lung

02-14-11

Ct scan of the brain (non-contrast axial-slice CT scan of the brain using 3 x 1.5 mm slices was done)


5/6

There is a hyperdense collection seen in the left parieto-occipital cortical-subcortical region measuring 5.4 x 4.0 x 5.2 cm and having

an approximately volume of 57 cc. There is perilesional edema with effacement of the overlying cortical sulci and compression of the occipital horn

of the left lateral ventricle. Minimal contralateral subfalcine midline shift is appreciated, measuring 0.5 cm.

Minimal intimal calcifications are seen in the bilateral carotid arteries.

Impression: acute intraperenchymal hemorrhage, left perieto-occipital cortical-subcotical region with mass effect as described.

Mild age cerebral volume loss

Atherosclerotic vessel disease.

>the hyperdense collection in the left parieto-occipital cortical-subcortical region is the accumulated hematoma caused by vesselrupture

>perilesional edema indicates the hematoma in the cortical sulci that compresses the occipital horn of the left lateral ventricle

>calcifications seen in the carotid arteries are atherosclerosis. The calcifications are the build up of fatty materials.

>there is a minimal change in position of a part of a brain towards the midline

02-25-11

CT scan of the Brain

Comparison is made with the previous study alone in another institutions dated Feb. 14, 2011.

The parenchymal hematoma in the left parietal lobe has about the same size, with approximate volume of 65 cc. There is however

an interval increase in the degree of edema with greater effacement of the lateral ventricle.

The third ventricle is now compressed causing dilatation of the lateral ventricles.

There is subfalcine herniation to the right about 1.4 cm.

Cortical sulci, sylvian fissures and basal cisterns are effaced.

>there is a bad progression of edema/hematoma formation on the cortical sulci, with the greater thinning of the tissue in the left

lateral ventricle.


6/6

>the third ventricle is a narrow vertical cleft between the two lateral vertical ventricles, filled with cerebrospinal fluid. Compression

of the CSF-filled third ventricle caused compression of nervous tissues and dilated the lateral ventricles, resulting in irreversible brain damage.

>sylvian fissures are cortical fissures that separate the frontal lobes and temporal lobes in both hemispheres. The basal cisterns are

wide cavities where the arachnoid extends across between the two temporal lobes. The two, together with the cortical sulci, are thinning.

>there is a change in position/herniation of a part of a brain towards the right

Zev - Laboratory and Diagnostic Evaluation

Documents

Transcript of Zev - Laboratory and Diagnostic Evaluation