Help me please  Marie Case Study 1 Scenario: Marie is a 27 year old female who is homeless. She arrives at the emergency department with

Help me please 

Marie Case Study 1

Scenario: Marie is a 27 year old female who is homeless. She arrives at the emergency

department with complaints pain in her left foot. After an assessment you discover that she has

an open wound on the bottom of her left foot that is red, swollen, and draining green fluid.

Cellulitis is present up the leg to the knee. She states she has no chronic medical illnesses and

doesn’t take any medication. She is alert and oriented to person, place and time. Her vitals are

BP: 100/78 (her normal is 120/80), Heart Rate 100, Temperature 100.5, Pulse Ox 98%,

respiratory rate is 22.

What condition are you suspecting?

Based on the symptoms presented—pain, redness, swelling, drainage of green fluid from the

foot, and cellulitis extending up to the knee—Marie is likely suffering from a severe bacterial

infection, possibly progressing to sepsis given the systemic symptoms (Salomão et al., 2019).

Does she have at least 2 criteria for Systemic Inflammatory Response Syndrome? If so, list

the criteria.

By the SIRS definition, Marie experiences the minimum grade of symptoms including a

temperature higher than the normal threshold and the heart rate that is greater than 90 bpm. For

instance, temperature is 100.5°F and the rate of the heart is 100 beats per minute. These

symptoms that point to her body fighting a major battle to recover from the infection and

possibly leading to septic shock (Otto, 2020).

What are your next steps?

Immediate actions should include (Otto, 2020):

• Continued monitoring of vital signs.

• Administering IV fluids and antibiotics.

• Preparing for possible escalation of care depending on the patient’s response.

What medication do you expect to be given, if any?

Antibiotics remain the basis for the treatment of bacteriological infections that help to

avoid further progress to sepsis. This would mean recommending suitable pain killers or

antipyretic drugs like aspirin for fever (Gyawali et al., 2019).

What labs do you expect the doctor to order?

The doctor is likely to order a complete blood count (CBC), blood cultures, lactate levels,

and other tests to assess the extent of the infection and organ function (Otto, 2020).

Is she improving?

Marie is not showing signs of improvement; her vital signs indicate worsening conditions

such as increased heart rate, respiratory rate, and fever. The chills and paleness could

suggest systemic infection progression (Salomão et al., 2019).

What do you expect the licensed practitioner to order?

The practitioner may order adjustments in antibiotic therapy based on culture results,

increased fluid administration, and potentially vasopressors if hypotension persists

(Gyawali et al., 2019).

If she was not improving, what would she be at risk for?

If Marie does not improve, she could be at risk for septic shock, organ failure, and

increased mortality (Gyawali et al., 2019).

What makes a person high risk for infection?

Factors include compromised immune system, chronic health conditions, wounds or injuries,

homelessness (exposure to unsanitary conditions), and lack of medical care (Otto, 2020).

Define sepsis.

Sepsis is an acute endogenous disease, caused by the body’s overall response to an infection

involving the development of damage to tissues, organs failure, and death (Gyawali et al., 2019).

In your own words, explain septic shock?

Septicemia (sepsis shock) is a severe state of an ill patient and blood pressure decrease occurs

secondary to septicemia by causing impaired metabolism in all body cells with septic

manifestations and multi-organ failure accompanied by extremely poor cardiovascular

metabolism and high mortality rate.

In your own words, explain the pathophysiology of Septic shock.

Septic shock results from the massive reaction of the immune system to an infection with

impaired normal organ and tissue function. The septic shock physiology involves different parts:

vessel dilatations, blood clot formations, and organ failures.

Give 2 examples of medications that can be used to treat Sepsis.

• Antibiotics: Essential for treating the underlying infection (Otto, 2020).

• Vasopressors: Used to stabilize blood pressure if fluid resuscitation is not sufficient

(Gyawali et al., 2019).

References

Gyawali, B., Ramakrishna, K., & Dhamoon, A. S. (2019). Sepsis: The evolution in definition,

pathophysiology, and management. SAGE open medicine, 7, 2050312119835043.

Otto, C. M. (2020). Sepsis. In The veterinary ICU book (pp. 695-709). CRC Press.

Salomão, R., Ferreira, B. L., Salomão, M. C., Santos, S. S., Azevedo, L. C. P., & Brunialti, M.

K. C. (2019). Sepsis: evolving concepts and challenges. Brazilian Journal of Medical and

Biological Research, 52, e8595.

Disseminated Intravascular Coagulation Case Study 2

Jerry is a 24 year old in the ICU that was hit by a car while walking 7 days ago. This

accident resulted He began to develop sepsis. Day 8 you notice petechiae on his torso and

blood oozing from his past IV insertion sites. His suture lines from his hip surgery are

oozing blood as well. Based on your assessment, you suspect disseminated intravascular

coagulation (DIC).

Explain why you suspected that Jerry developed DIC (scenario data and textbook

support)?

Elevating the probability of DIC in Jerry’s case is based on pivotal signs noted in the case. First

of all, the occurrence of petechiae on his torso and bleeding from past venous cannulation sites

and suture lines signify the abnormal tendency of bleeding, characteristic feature for DIC (Lehne

& Rosenthal, 2019). Besides that, Jerry’s previous trauma experience from being hit by a car

could have initiated a domino effect that led to DIC. Trauma is the main cause of DIC, where

disintegration of cells and release of procoagulant compounds in blood overload the body system

by shutting off the vital anticoagulants mechanisms. This results in microvascular thrombosis

and depletion of clotting factors and platelets with the sequel of bleeding (Keohane et al., 2019).

Define Disseminated Intravascular Coagulation.

Disseminated intravascular coagulation (DIC) is characterized by systemic activation of

coagulation cascade leading to thrombi and hemorrhages. Generally, it is the state where the

body’s clotting response becomes hyperactive, and therefore, multiple small clots form in the

blood vessels (Keohane et al., 2019). These clots are destructive to organs and tissues and

simultaneously denies the body more and more clotting factors and platelets, causing a bleeding

tendency.

What labs do you expect to be ordered?

Jerry’s diagnosis of DIC could probably be confirmed by through some laboratory tests in order

determine its severity. Per Smith (2021), these may include:

• Complete Blood Count (CBC) with platelet count

• Prothrombin Time (PT) and Partial Thromboplastin Time (PTT)

• Fibrinogen levels

• D-dimer assay

• Peripheral blood smear

With each lab value, indicate if that value would be abnormally high or low for a pt.

with DIC and explain.

In DIC, testing laboratory often shows abnormalities which show elements of both

thrombosis and hemorrhage. According to Smith (2021), these are specifically:

• • Platelet count: Initially high platelet counts are observed due to the platelet activation

and consumption, but as DIC progresses, thrombocytopenia (low platelet count) develops

due to continued platelet destruction.
• PT and PTT: These values can be maintained over a longer period of time with additional

clotting factors.
• Fibrinogen: Initially high due to acute phase response, but the tendency reverses as DIC

progresses with fibrinogen level falls due to incessant consumption in clot formation.

• D-dimer: Elevation resulting from clot degradation mediated via fibrinolysis. What is the

pathophysiology causing the change in lab values?

The pathogenesis of DIC is based on the activation of the coagulation cascade via different

triggers that could be related to trauma, sepsis, or obstetrical problems. These triggers

consequently initiate the process that produces thrombin, which subsequently converts

fibrinogen into fibrin and causes the development of microthrombi in vasculature (Lehne &

Rosenthal, 2019). Concurrently with the contribution of coagulation factors and platelets in

microthrombi formation, the coagulopathy is disrupted and the patient becomes more prone to

bleeding.

What are patients with DIC at risk for due to the abnormally high consumption of clotting

factors and platelets and why?

Patients with DIC often develop complications that may progress to organ dysfunction or multi-

organ failure ultimately due to the formation of microvascular thrombosis leading to eventual

tissue damage. Moreover, the plasma elements important in clotting like clotting factors and

platelets can be reduced leading to severe hemorrhage and bleeding from several sites that may

be fatal when if treated on time (Keohane et al., 2019).

How is DIC managed?

The management of DIC involves addressing the root cause along with providing supportive care

so as to manage the bleeding and thrombotic complications. According to Lehne & Rosenthal

(2019), treatment may include:

• Management of the cause like sepsis or traumatic injuries is essential.

• Transferring blood products like platelets, fresh-frozen plasma, and cryoprecipitate to

correct clotting abnormalities.

• Anticoagulant therapy for selected patients to hinder future thrombin generation.

• Measures including mechanical ventilation and the management of organ failure with

hemodynamic support will also be employed.

• Regularly checking laboratory values and clinical status to guide management decision

making.

References

Keohane, E. M., Otto, C. N., & Walenga, J. M. (2019). Rodak’s Hematology-E-Book: Rodak’s

Hematology-E-Book. Elsevier Health Sciences.

Lehne, R. A., & Rosenthal, L. (2019). Pharmacology for Nursing Care-E-Book. Elsevier Health

Sciences.

Smith, L. (2021, April). Disseminated intravascular coagulation. In Seminars in oncology

nursing (Vol. 37, No. 2, p. 151135). WB Saunders.

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