Clinical Presentation of Disseminated Intravascular Coagulation in the Clinic of Internal Diseases

1. Samatbek Turdaliev

2. Gurjar Rahul

Joshi Tanuja

(1 Teacher, International Medical Faculty, Osh State University, Osh, Kyrgyz Republic.

2. Students, International Medical Faculty, Osh State University, Osh, Kyrgyz Republic.)

Abstract

Disseminated intravascular coagulation (DIC) remains a complex clinical syndrome encountered across numerous internal medicine settings, distinguished by widespread activation of the coagulation cascade, consumption of platelets and clotting factors, and paradoxical coexistence of thrombosis and bleeding. Its clinical presentation is often heterogeneous, evolving from subtle laboratory abnormalities to fulminant multi-organ dysfunction, thereby demanding a high index of suspicion among clinicians. This article provides a comprehensive overview of how DIC clinically manifests in the clinic of internal diseases, emphasizing its pathophysiological basis, characteristic features, diagnostic challenges, and implications for patient outcomes. By examining the varied presentations seen in adult patients with underlying infections, malignancies, liver disease, obstetric complications, and catastrophic systemic disorders, the paper highlights the crucial importance of early recognition. The narrative is grounded in classical internal medicine practice, synthesizing current understanding with practical clinical observations, and exploring how DIC’s protean manifestations merge into the everyday diagnostic and therapeutic dilemmas confronted by physicians.

Introduction

Disseminated intravascular coagulation represents one of the most compelling yet intimidating clinical syndromes in internal medicine. It is not a disease in itself but a pathophysiological process triggered by diverse primary conditions that lead to widespread coagulation activation. Internal medicine physicians frequently engage with patients whose conditions set the stage for DIC: severe bacterial infections such as sepsis, metastatic cancers, major trauma, liver cirrhosis, autoimmune disorders, and complications of chronic illnesses that destabilize homeostasis. Because of this broad etiological spectrum, the clinical presentation of DIC varies remarkably, often creating diagnostic uncertainty. For many clinicians working in internal disease clinics, DIC is an ever-present possibility—sometimes silent and chronic, at other times rapidly fatal.

Despite decades of research, DIC continues to challenge clinical judgment. Its manifestations intersect with nearly every organ system, and the symptoms can be deceptively nonspecific at the onset. Fatigue, mild bleeding tendencies, subtle petechiae, or unexplained hypotension may be the earliest clues. In other cases, the presentation is abrupt, marked by sudden hemodynamic collapse, uncontrollable bleeding, or ischemic limb changes. In the clinic of internal diseases, where chronic diseases and complex multisystem interactions are routine, recognizing DIC requires a nuanced understanding of how systemic pathology expresses itself on the coagulation system.

This article aims to explore the clinical presentation of DIC specifically in the context of internal medicine practice. While the pathophysiology is universally applicable, the manifestations encountered in outpatient clinics, hospital wards, and emergency consultations within internal medicine often differ from those observed in surgical or obstetric units. The slow progression of malignancy-associated DIC, the fluctuating coagulation status in cirrhotic patients, the sudden deterioration of septic individuals, and the diagnostic difficulties in patients with chronic inflammatory diseases exemplify the challenges faced by internists. Through a detailed discussion structured in IMRAD format, this paper delineates the typical and atypical manifestations of DIC, correlates them with underlying disease processes, and draws attention to clinical patterns that may support earlier diagnosis.

Methods

This article adopts a narrative review-style methodological approach, synthesizing established medical knowledge, classical internal medicine teaching, and clinically relevant patterns documented in peer-reviewed medical literature. Rather than conducting a systematic review, the method involves the integration of observational insights drawn from internal medicine practice with current theoretical models of DIC pathogenesis and clinical expression. Emphasis is placed on understanding how DIC presents across various internal disease scenarios, acknowledging the variation between acute and chronic forms, and interpreting findings within the day-to-day context of adult patient management.

The analysis is structured by reviewing the predominant etiological categories encountered in internal medicine—sepsis, malignancy, liver disease, autoimmune pathology, and systemic inflammatory states—and examining how DIC manifests clinically within each scenario. Laboratory patterns and diagnostic reasoning are described based on recognized criteria, but all interpretations are presented in a non-prescriptive manner, avoiding actionable medical instructions. The goal of this methodological framework is to illustrate patterns of presentation rather than define clinical guidelines, thereby producing a descriptive academic piece suitable for undergraduate and postgraduate learning environments.

Results

1. Pathophysiological Context in Internal Medicine

In the internal diseases clinic, the pathogenesis of DIC is often rooted in systemic conditions that exert prolonged or intense stress on the coagulation system. Infectious diseases, particularly sepsis caused by gram-negative and gram-positive organisms, remain a frequent driver, with endotoxins and inflammatory mediators such as interleukin-6 and tumor necrosis factor-alpha stimulating widespread tissue factor expression. Malignancy presents another major trigger; certain tumors such as pancreatic, gastric, or prostate cancers release procoagulant substances that activate coagulation chronically. Liver disease contributes by impairing the synthesis of both procoagulant and anticoagulant proteins, disrupting balance in a way that predisposes the patient to DIC when additional stress arises. Autoimmune diseases offer yet another pathway, where persistent inflammation fosters endothelial damage and thrombin generation.

Across these diverse scenarios, the unifying feature is the dysregulated activation of coagulation that consumes platelets and clotting factors. Microthrombi begin forming in the microvasculature, especially in the kidney, liver, lungs, and brain. As the process accelerates, fibrinolysis may be suppressed or activated excessively, adding further complexity. This dynamic imbalance between clot formation and clot breakdown sets the stage for the characteristic clinical picture of DIC: a simultaneous tendency toward thrombosis and bleeding, each driven by a different phase of the same underlying process.

2. General Clinical Presentation

In internal medicine, the presentation of DIC frequently begins subtly. Patients may complain of unexplained bruising or exhibit scattered petechiae on examination, often mistaken initially for thrombocytopenia of other origins. Mild mucosal bleeding—such as gum bleeding during tooth brushing or epistaxis—may precede more visible hemorrhage. Fatigue, malaise, and progressive pallor can develop as anemia emerges secondary to bleeding or hemolysis associated with microvascular injury. In acute DIC, however, the transformation from minor symptoms to life-threatening manifestations can occur within hours, especially in septic patients or those with severe systemic inflammation.

Bleeding tends to stand out as the most dramatic clinical feature. Oozing from venipuncture sites, prolonged bleeding from minor injuries, hematuria, hematemesis, melena, or heavy menstrual bleeding may occur. In hospitals, clinicians may notice that intravenous lines or catheter sites bleed persistently, a characteristic sign that raises suspicion for consumptive coagulopathy. However, bleeding severity varies widely; in chronic DIC, bleeding may be minimal or absent altogether.

Thrombotic manifestations form the other pillar of the syndrome. In many internal medicine patients, thrombotic signs may actually appear before bleeding becomes evident. Deep vein thrombosis, digital ischemia, renal dysfunction due to microvascular thrombosis, or evidence of pulmonary involvement may all develop insidiously. Some patients report numbness or burning pain in extremities, symptoms that may easily be misattributed to diabetic neuropathy or vascular disease until further evidence emerges.

3. Clinical Presentation in Specific Internal Disease Settings

a. Sepsis-Related DIC

Sepsis represents one of the most common and severe causes of DIC in adult internal medicine practice. The clinical presentation in such patients is often rapid and overwhelming. Fever, altered mental status, tachypnea, and hypotension usually precede coagulopathic signs. As the systemic inflammatory response intensifies, patients may develop purpura fulminans—a frightening manifestation characterized by rapidly spreading bruising and skin necrosis due to microvascular thrombosis. In this context, bleeding tends to be widespread, involving gastrointestinal, respiratory, and genitourinary systems. The combination of hemodynamic instability with visible hemorrhage often prompts urgent laboratory evaluation, which typically reveals prolonged PT/aPTT, markedly reduced platelets, and elevated D-dimers.

b. Malignancy-Associated DIC

Patients with advanced cancers frequently develop a chronic form of DIC that presents more subtly. Rather than dramatic bleeding, these patients often experience gradually worsening fatigue, frequent bruising, and occasional mucosal bleeding. Thrombosis is a more dominant feature, consistent with the broader hypercoagulable state seen in malignancy. Some may present with migratory thrombophlebitis, unexplained renal insufficiency, or persistent laboratory disturbances such as elevated fibrin degradation products. Because the progression is slow, clinicians may initially attribute these findings to the malignancy itself or to chemotherapy complications. Only when bleeding becomes more prominent—often due to a secondary insult such as infection—does the underlying DIC become clinically obvious.

c. DIC in Liver Disease

Liver disease introduces unique challenges in diagnosing DIC because many laboratory abnormalities overlap. Patients with cirrhosis already exhibit elevated PT/INR, thrombocytopenia, and splenomegaly, which can obscure early DIC. Clinically, they may present with worsening ascites, gastrointestinal bleeding such as variceal hemorrhage, or spontaneous bacterial peritonitis that triggers DIC. Confusion and hepatic encephalopathy may complicate the picture further. In these patients, the emergence of new petechiae, excessive bleeding from minor procedures, or sudden kidney injury may be early clues that DIC has superimposed itself on the pre-existing coagulopathy.

d. Autoimmune and Inflammatory Diseases

In systemic lupus erythematosus, rheumatoid arthritis, and vasculitis disorders, chronic inflammation predisposes to endothelial injury and coagulation abnormalities. When DIC develops, the presentation may mimic an acute flare of the underlying disease. Patients may report worsening joint pain, skin lesions, fatigue, and organ involvement. Skin manifestations such as palpable purpura or digital ischemia may reflect microthrombi. Because bleeding is often minimal in these cases, the diagnosis may be delayed unless clinicians consider DIC as a potential complication of systemic inflammation.

e. DIC in Endocrine and Metabolic Disorders

Although less common, conditions such as severe pancreatitis, diabetic ketoacidosis, and thyroid storm encountered in internal medicine can trigger DIC. Here, the presentation is often dominated by the acute metabolic crisis, and coagulopathy emerges as the disease progresses. Patients may show bluish discoloration of extremities due to microvascular obstruction, oozing from injection sites, or laboratory findings that become progressively deranged. These manifestations emphasize the importance of monitoring coagulation parameters in severe metabolic derangements.

4. Organ System Involvement

The presentation of DIC frequently reflects multi-organ dysfunction. Renal involvement manifests as oliguria or rising creatinine levels due to microthrombi obstructing renal vasculature. Pulmonary consequences include shortness of breath, hypoxia, or acute respiratory distress syndrome when inflammatory and thrombotic processes converge. Neurological symptoms range from confusion and agitation to seizures or coma in severe cases, often resulting from cerebral micro thrombosis or hemorrhage. Dermatological manifestations, ranging from petechiae to large ecchymoses, remain among the most visible and diagnostically helpful signs.

5. Laboratory Presentation

Though the focus of this article is the clinical presentation, laboratory findings support the interpretation of symptoms. In the internal medicine clinic, key abnormalities include thrombocytopenia, prolonged PT and aPTT, low fibrinogen, and elevated D-dimer levels. Chronic DIC may show only modest abnormalities, which fluctuate over time. Clinicians often discover these changes during routine evaluations for anemia, infection, or treatment monitoring, highlighting how laboratory data often reveal DIC before symptoms become pronounced.

Discussion

DIC remains a formidable diagnostic and therapeutic challenge in internal medicine because its presentation is deeply intertwined with the primary illness triggering it. Its protean manifestations—ranging from subtle bruising to catastrophic hemorrhage—parallel the severity and progression of underlying systemic disease. Internal medicine clinicians must therefore maintain a high index of suspicion, especially when evaluating patients with sepsis, malignancy, chronic liver disease, or autoimmune conditions.

This narrative exploration of DIC presentation underscores that the syndrome rarely announces itself in a straightforward fashion. Instead, its clinical picture unfolds gradually or suddenly depending on the balance between thrombotic and hemorrhagic forces at play. Acute DIC tends to overwhelm the patient rapidly, often revealing itself through widespread bleeding, hemodynamic compromise, and multi-organ dysfunction. Chronic DIC, more commonly seen in cancer or chronic inflammatory disorders, presents as a quieter but persistent pattern of thrombosis and intermittent bleeding, often masked by the symptoms of the underlying disease.

The internal medicine context adds layers of complexity to recognition. Many patients have multiple comorbidities—diabetes, hypertension, renal insufficiency, long-standing infections, or malnutrition—that obscure the presentation or mimic its symptoms. For example, kidney injury in a septic patient might initially appear due to dehydration or medication effects, delaying recognition of DIC-related microvascular thrombosis. Similarly, bruising in a cancer patient undergoing chemotherapy may be attributed to treatment-induced cytopenias unless clinicians consider DIC as an additional contributor.

Clinical awareness must therefore extend beyond the classic textbook description of DIC. Recognizing atypical presentations—subtle cognitive changes, persistent low-grade bleeding, unexplained skin lesions, or fluctuating laboratory findings—can prompt earlier investigation. Understanding the patient’s broader medical context becomes essential: each case of DIC carries the signature of its underlying cause. In sepsis, for instance, the inflammatory cascade accelerates rapidly, leading to fulminant DIC. In malignancy, chronic activation of coagulation produces a different, more indolent picture. Recognizing these patterns improves diagnostic sensitivity and helps differentiate DIC from other coagulopathies.

Another crucial point highlighted by internal medicine practice is that DIC rarely presents without laboratory clues. Even when clinical manifestations are muted, abnormalities such as rising D-dimer levels or declining platelet counts may signal early DIC. For this reason, clinicians caring for high-risk patients often monitor coagulation parameters routinely, allowing them to identify shifts that could precede clinical deterioration. While laboratory data alone cannot diagnose DIC, they help contextualize clinical signs and support the overall interpretation of the patient’s condition.

Ultimately, understanding the clinical presentation of DIC in internal diseases involves more than reciting diagnostic criteria. It demands a nuanced interpretation of symptoms within the complex and often ambiguous clinical environment of internal medicine. It requires awareness of underlying diseases, recognition of subtle shifts in patient status, and appreciation of the body’s fragile balance between clotting and bleeding. The varied manifestations of DIC reflect the systemic turmoil within the patient, and early recognition can influence outcomes substantially.

Conclusion

Disseminated intravascular coagulation remains a compelling clinical entity encountered across the spectrum of internal medicine. Its presentation is highly variable, shaped by the underlying disease, the patient’s physiological reserve, and the dynamic interplay between coagulation and inflammation. In the internal medicine clinic, DIC often presents as a complex diagnostic puzzle, requiring clinicians to integrate subtle clinical clues with supportive laboratory evidence. Whether unfolding as acute, life-threatening hemorrhage or as a chronic, insidious coagulopathy, DIC reflects systemic pathology that demands swift recognition.

Through understanding the patterns of presentation described in this article, clinicians and students of internal medicine can cultivate a deeper appreciation for how DIC manifests in real-world practice. This knowledge empowers them to recognize early signs, interpret ambiguous symptoms, and maintain vigilance in high-risk patients. Given the significant morbidity associated with DIC, improved recognition remains a fundamental component of patient care in internal diseases.

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