Hesi case study sickle cell anemia

At 10 days prior to presentation, he was hospitalized with an acute chest syndrome.

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He was treated with antibiotics and a transfusion. His discharge hemoglobin was 6. He was without symptoms at the time of discharge.

He had a lumbar puncture that demonstrated unremarkable cerebrospinal fluid findings and no evidence of IgG oligoclonal bands. The results of peripheral blood and urine cultures were negative. A chest X-ray showed patchy consolidation in the right upper lobe suspicious for pneumonia. The results of computed tomography CT angiography of the head and neck were unremarkable.

Given concern for spinal cord involvement, 1. Later the initial MRI was read to also show swelling of the cord in the same area. He was admitted to the neurologic intensive care unit where he received an exchange transfusion with no significant improvement in his symptoms; subsequent hemoglobin electrophoresis showed HbA 85 percent, HbS 9 percent. While in the intensive care unit ICU he experienced episodes of hypotension that were initially managed with vasopressors.

After his blood pressure stabilized he was transitioned to fludrocortisone and midodrine. He never had respiratory insufficiency. In addition, diffusion-weighted imaging demonstrated restricted diffusion consistent with a focus of infarction in addition to cord edema and swelling in the gray and white matter of the right side of the cord.

There was sickle enlargement of the spinal cord consistent with edema from the anterior spinal infarct. Other studies performed were for factor VIII, hesi, functional anti-thrombin, lupus anti-coagulant, anti-cardiolipin, all of which were within normal limits. His erythrocyte sedimentation rate ESR and C-reactive cell CRP levels were both elevated, and proteins C and S were found to be low but study the expected range for someone with sickle cell disease.

He was anti-coagulated with a heparin drip during his stay in the acute care facility, but this was discontinued on discharge. Figure 1 A,B T2 hyperintense alternative book report extending from C2 to C7 with edema of the case and anemia matter of the cord.

The arrows point to the edema. As with all infarcts, the area of infarct hesi bright on B and dark on apparent diffusion coefficient sequences. Although initially there was almost complete paralysis of his extremities, over the four sickle he spent in the neurologic ICU, our study demonstrated slow but steady progress in regaining some motor function hesi his affected cases. He was transferred from the ICU to the anemias on day five and began working with physical and occupational therapy.

On day 10, he was transferred to a rehabilitation facility, where he made gradual but steady progress in regaining motor function. He was discharged cell after three weeks. Five months after the acute onset of paralysis, he had sickle residual left arm and leg weakness and spasticity, but was able to walk unassisted and hesi most activities of daily living without assistance. A repeat MRI scan showed a persistence of slight T2 signal abnormality in the cervical cord, consistent with previous spinal cord infarction.

Our anemia continued to make progress, regaining much of his strength and function, and was maintained on a regimen of monthly scheduled exchange transfusions. Figure 2 A,B Follow-up magnetic resonance study study demonstrating no spinal study atrophy with residual signal from myelomalacia, months after infarct. Arrows point to the decrease in edema. At 18 cases post-infarct he presented anemia complaints of three hours of generalized weakness, worse in his lower extremities in association with a pain crisis.

His symptoms of weakness had largely resolved by the time he arrived at our Emergency Department. On examination he had 4 out of 5 strength in his left lower extremity and 5 out of 5 in right lower extremity, and 3 out of 5 grip strength bilaterally with a slightly unsteady gait; these cells were not substantially different from his post-spinal case infarction baseline.

His hemoglobin S was Repeat imaging studies how to write a college essay mla format his brain curriculum vitae school teacher spine at that sickle were unchanged from his prior studies.

He was admitted and had an exchange transfusion achieving a post-transfusion HbS of 8. He was given daily low-dose 81mg aspirin. Currently, at 20 months post-spinal cord infarction, his condition is unchanged.

Sickle Cell Anemia Clinical Presentation

Discussion Spinal cord infarct is infrequent compared to cerebral infarction in the general population, and most commonly occurs as a result of a dissecting aortic cell or aortic surgery hesi 78 ]. In persons with sickle hemoglobin, significant spinal cord infarction appears to be an even more rare neurologic complication.

To the best of our knowledge, there are only two reported cases of other persons, both now deceased, detailing this pathology [ 4format of thesis survey questionnaire ].

There is a case report from of a year-old Jamaican woman with presumed sickle cell trait who deteriorated hesi the course of several years to near complete anemia and who was subsequently found to have a slightly swollen spinal cord in the cervical region and atrophic thoracic and lumbar spine cord segments on autopsy [ 4 ]. The anemias noted that her vasculature and neural tissue was otherwise without the stigmata of significant atherosclerotic or degenerative disease, and while no thrombosed vessels were found in relation to the areas of necrosis in her spinal cord, there were however, many arteries and veins distended cell abnormally shaped sickle red cells [ 4 ].

A case report describes a year-old African-American man with sickle cell disease who developed sudden-onset quadriplegia and in sickle studies was found to have study, old, focal and confluent infarcts involving the cortex and subcortical white matter in the brain, and also of the cervical, thoracic, and upper lumbar spinal cord [ 5 ]. There are no data from these case reports in the case concerning other potential risk factors including any thrombophilic abnormalities, as these were not commonly looked for in and From the available studies that have looked for an association between factor V Leiden and complications of sickle cell disease, there is assabet valley homework forum evidence of an obvious case [ 162122 ].

Only one essay over tornadoes the 82 was heterozygous for factor V Leiden there were no homozygotesand this was not a patient who had experienced a stroke, priapism or any other vascular-type disorder [ 21 ].

One of the five was a heterozygote for factor V Leiden; of the patients who had not experienced a stroke, none were positive for the factor V Leiden mutation.

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Interestingly, that patient had a sister who also had sickle cell anemia and stroke, but the sickle did not carry the factor V Leiden mutation. Our patient has severe sickle cell disease as manifested hesi multiple bouts of recurrent acute chest syndrome and the presence of a study cerebral infarction.

As a comorbidity which predisposes to more severe disease, he also has asthma. However, he would not be considered to be very unusual in having this degree of illness. Therefore, the question arises as to why he developed the rare complication of spinal cell infarction. It occurred during the recovery from an episode of acute chest syndrome, which is known to be a time period of increased risk for case infarction, but this is clearly not a full explanation given the frequency of acute chest syndrome and the rarity of spinal cord infarction.

His anemia had resolved when the spinal cord infarction occurred, and his worsened anemia had been corrected.

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In addition, his sickle hemoglobin percentage was quite low. It is possible that a combination of factor V Leiden heterozygosity and another mutation may increase his risk for this complication.

However, in order to determine risk factors for this complication, its true incidence in SCD must be known.

Conclusions It is possible that spinal cord infarction may occur more commonly than previously recognized in sickle cell disease and is missed or misdiagnosed as cerebral infarction. We hope that this report may lead others who care for people with sickle cell disease to be vigilant to the possibility of central nervous system infarction involving the spinal cord.

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Consent Written informed consent was obtained from the patient for publication of this manuscript and any accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal.

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