# Situation: A 68-year-old woman weighing 60 kg is admitted to the intensive care unit (ICU) with fever, flank pain, and confusion from an acute kidney infection. Her temperature is 39.4 °C, heart rate 124/min, respiratory rate 28/min, blood pressure 82/44 mmHg (mean arterial pressure 57 mmHg), and serum lactate 4.8 mmol/L (43 mg/dL). On day 2, blood oozes from her intravenous and arterial line sites, and her fingertips are cool and dusky. She started subcutaneous heparin prophylaxis on admission and had not received heparin before this illness. Her results are: Platelet count: 48 × 10⁹/L (normal 150–400 × 10⁹/L) Prothrombin time: prolonged; international normalized ratio (INR) 2.1 Activated partial thromboplastin time (aPTT): prolonged Fibrinogen: 0.9 g/L (normal 2.0–4.0 g/L) D-dimer: markedly elevated Which condition do these findings MOST likely indicate?

> source: MyMerci (mymerci.kr)  
> url: https://mymerci.kr/pages/nclex_q.php?qn_id=629889  
> language: ko  
> subject: Nursing Practice III — Care of Clients with Problems in Surgery, Oxygenation, Fluid and Electrolytes, Infectious, Inflammatory and Immunologic Response, Cellular Aberrations

## 문제

Situation: A 68-year-old woman weighing 60 kg is admitted to the intensive care unit (ICU) with fever, flank pain, and confusion from an acute kidney infection. Her temperature is 39.4 °C, heart rate 124/min, respiratory rate 28/min, blood pressure 82/44 mmHg (mean arterial pressure 57 mmHg), and serum lactate 4.8 mmol/L (43 mg/dL).

On day 2, blood oozes from her intravenous and arterial line sites, and her fingertips are cool and dusky. She started subcutaneous heparin prophylaxis on admission and had not received heparin before this illness. Her results are:
Platelet count: 48 × 10⁹/L (normal 150–400 × 10⁹/L)
Prothrombin time: prolonged; international normalized ratio (INR) 2.1
Activated partial thromboplastin time (aPTT): prolonged
Fibrinogen: 0.9 g/L (normal 2.0–4.0 g/L)
D-dimer: markedly elevated
Which condition do these findings MOST likely indicate?

## 보기

1. Vitamin K deficiency from antibiotics and poor intake
2. Disseminated intravascular coagulation from sepsis **✔ 정답**
3. Heparin-induced thrombocytopenia with new thrombosis
4. Immune thrombocytopenia triggered by the infection

**정답: 2**

## 해설

Sepsis can trigger widespread clotting in small vessels that consumes platelets and clotting factors and activates fibrinolysis. The result is bleeding (oozing from line sites) and clotting (dusky fingertips) at the same time, with low platelets and fibrinogen, prolonged prothrombin time and aPTT, and a high D-dimer. Only disseminated intravascular coagulation explains all five abnormal results; heparin-induced thrombocytopenia is unlikely on day 2 of a first heparin exposure and does not lower fibrinogen or prolong clotting times.

## 심화 해설

Core Pathophysiology

Sepsis drives a systemic inflammatory response that massively upregulates tissue factor on monocytes and endothelial cells. This triggers thrombin generation throughout the microcirculation, forming fibrin-rich microthrombi in small vessels. At the same time, the sustained coagulation consumes platelets, fibrinogen, and clotting factors, while secondary fibrinolysis degrades the fibrin that has formed. The clinical result is a paradoxical combination: microvascular thrombosis causing end-organ ischemia, alongside a bleeding tendency from depletion of hemostatic components [1][2].

In this patient, the cool, dusky fingertips reflect microvascular occlusion in the skin, while oozing from intravenous and arterial line sites reflects the consumptive coagulopathy. The laboratory profile fits this dual process: platelets 48 × 10⁹/L, fibrinogen 0.9 g/L, prolonged PT/INR 2.1, prolonged aPTT, and markedly elevated D-dimer. No single alternative in the options explains all five abnormalities simultaneously [1][3].

Why the Other Options Do Not Fit

| Condition | Platelets | Fibrinogen | PT/aPTT | D-dimer | Key Discordant Finding |
| --- | --- | --- | --- | --- | --- |
| Vitamin K deficiency | Normal | Normal | Prolonged | Normal or mildly elevated | Does not consume platelets or fibrinogen; no microthrombosis |
| Heparin-induced thrombocytopenia (HIT) | Low | Normal | Normal | Normal or mildly elevated | Thrombosis without hypofibrinogenemia or prolonged clotting times |
| Immune thrombocytopenia (ITP) | Low | Normal | Normal | Normal | Isolated platelet destruction; no consumption coagulopathy |
| Disseminated intravascular coagulation (DIC) | Low | Low | Prolonged | Markedly elevated | Matches all five abnormalities |

Watch out! HIT typically develops 5–14 days after first heparin exposure, not on day 2. Even when HIT causes thrombosis, it does not lower fibrinogen or prolong the PT/aPTT, because it is an antibody-mediated platelet activation disorder, not a consumptive coagulopathy [2].

Sepsis-Induced Coagulopathy and DIC as a Spectrum

Current understanding frames sepsis-associated coagulopathy as a continuum. Early compensated activation may show only mild laboratory changes, but as the process advances, overt DIC emerges with the classic picture of thrombocytopenia, hypofibrinogenemia, prolonged global clotting times, and high fibrin degradation products. The ISTH overt DIC criteria rely on exactly these parameters, which is why a septic patient with this combination should be recognized as having overt DIC rather than a milder coagulopathy [3].

Key point! In sepsis, DIC is not a separate disease but the end-stage consumptive phase of infection-driven coagulation. The primary management is source control and antimicrobial therapy for the underlying infection, with supportive blood product replacement guided by bleeding risk and laboratory trends [3].

Putting the Clinical Picture Together

The patient’s presentation of fever, flank pain, confusion, hypotension with a MAP of 57 mmHg, tachycardia, tachypnea, and lactate 4.8 mmol/L establishes septic shock from a urinary source. The subsequent development of simultaneous bleeding and microvascular thrombosis, combined with the five characteristic laboratory derangements, is the defining signature of DIC. A low platelet count alone would not distinguish DIC from HIT or ITP; it is the concurrent fall in fibrinogen with prolonged PT and aPTT and a markedly elevated D-dimer that confirms consumptive coagulopathy [1][2].
References (research sources)

- [1]Disseminated intravascular coagulation.Research articleGando S, Levi M, Toh CH (2016) · DOI: 10.1038/nrdp.2016.37

- [2]Disseminated intravascular coagulation: epidemiology, biomarkers, and management.Research articleAdelborg K, Larsen JB, Hvas AM (2021) · DOI: 10.1111/bjh.17172

- [3]Sepsis-Induced Coagulopathy and Disseminated Intravascular Coagulation.Research articleIba T, Levi M, Levy JH (2020) · DOI: 10.1055/s-0039-1694995

## 임상 시나리오

Sepsis-Induced DIC: Recognition and ManagementWhen bleeding and clotting coexist in critical illness
Suspect disseminated intravascular coagulation when a septic patient develops simultaneous bleeding from line sites and microvascular thrombosis such as dusky, cool extremities. The hallmark laboratory pattern includes thrombocytopenia, hypofibrinogenemia, prolonged PT/aPTT, and markedly elevated D-dimer.

The primary treatment is source control of the underlying infection with appropriate antibiotics and hemodynamic support. Transfusion of platelets, fresh frozen plasma, or cryoprecipitate is reserved for active bleeding or high-risk procedures, not for laboratory abnormalities alone.

CautionDo not confuse DIC with heparin-induced thrombocytopenia, which typically occurs after 5–10 days of heparin exposure and does not cause hypofibrinogenemia or prolonged clotting times. In DIC, heparin prophylaxis alone does not stop the underlying consumptive process.

## 핵심 개념

- **Disseminated intravascular coagulation (DIC)** — A consumptive coagulopathy triggered by systemic inflammation (e.g., sepsis) causing widespread microvascular thrombosis and bleeding due to depletion of platelets, fibrinogen, and clotting factors.
- **Consumptive coagulopathy** — A state in which ongoing coagulation depletes platelets and clotting factors, leading to a bleeding tendency despite excessive clot formation.
- **D-dimer** — A fibrin degradation product that is markedly elevated in DIC due to secondary fibrinolysis of microvascular thrombi.
- **Heparin-induced thrombocytopenia (HIT)** — An immune-mediated reaction to heparin causing platelet activation and thrombosis, typically occurring after 5–10 days of exposure, without hypofibrinogenemia or prolonged PT/aPTT.
- **Microvascular thrombosis** — Clot formation in small vessels that impairs tissue perfusion, as seen in the cool, dusky fingertips of this patient with DIC.

## 같은 주제 문제

- [Situation: A 24-year-old woman with asthma is brought to the emergency room (ER) with whee…](https://mymerci.kr/pages/nclex_q.php?qn_id=629676)
- [Situation: A 24-year-old woman with asthma is brought to the emergency room (ER) with whee…](https://mymerci.kr/pages/nclex_q.php?qn_id=629677)
- [Situation: A 24-year-old woman with asthma is brought to the emergency room (ER) with whee…](https://mymerci.kr/pages/nclex_q.php?qn_id=629678)
- [Situation: A 24-year-old woman with asthma is brought to the emergency room (ER) with whee…](https://mymerci.kr/pages/nclex_q.php?qn_id=629679)
- [Situation: A 36-year-old woman comes to the Rural Health Unit (RHU), which provides free t…](https://mymerci.kr/pages/nclex_q.php?qn_id=629680)
- [Situation: A 36-year-old woman comes to the Rural Health Unit (RHU), which provides free t…](https://mymerci.kr/pages/nclex_q.php?qn_id=629681)
- [Situation: A 36-year-old woman comes to the Rural Health Unit (RHU), which provides free t…](https://mymerci.kr/pages/nclex_q.php?qn_id=629682)
- [Situation: A 22-year-old tall, thin man who smokes is admitted to the surgical ward with a…](https://mymerci.kr/pages/nclex_q.php?qn_id=629683)

---

More free questions: [기출문제](https://mymerci.kr/)

_학습 참고용입니다. 실제 임상은 최신 지침과 소속 기관 프로토콜을 따르세요._