Kehr sign is defined clinically as the development of acute, severe referred pain localized to the left shoulder tip, resulting from noxious mechanical or chemical irritation of the inferior surface of the diaphragm 2,3. First described by the German surgeon Hans Kehr, this classical clinical sign serves as a vital bedside indicator of underlying hemoperitoneum, most frequently triggered by blunt or iatrogenic splenic rupture, ectopic pregnancy rupture, or acute intraperitoneal inflammation 2,3. Because visceral afferent fibers lack precise spatial localization within the cerebral cortex, irritation of the central diaphragmatic peritoneum—innervated by the somatic motor and sensory fibers of the phrenic nerve (C3-C5)—is relayed centrally to the cervical spinal cord segments that simultaneously receive cutaneous sensory input from the ipsilateral supraclavicular region (C3-C4) 2,3. Recognizing Kehr sign during the physical examination of a trauma victim, a post-procedural patient following diagnostic colonoscopy, or an individual presenting with spontaneous abdominal discomfort is paramount for preventing delayed diagnosis of life-threatening intra-abdominal hemorrhage 2,3.

Etiology & Risk Factors

  • Traumatic Splenic Injury: Blunt abdominal trauma resulting from motor vehicle collisions, contact sports injuries, or direct falls onto the left lower chest wall and upper abdomen 2,3.
  • Iatrogenic Splenic Rupture: Procedural complication arising secondary to diagnostic colonoscopy, therapeutic polypectomy, bariatric surgery, or left-sided upper gastrointestinal endoscopic maneuvers that place traction on the splenocolic ligament 2.
  • Spontaneous Splenic Pathology: Pathological rupture occurring in a previously normal or pathologically enlarged spleen due to infectious mononucleosis (Epstein-Barr virus), malaria, cytomegalovirus, amyloidosis, or hematologic malignancies (e.g., acute leukemias, lymphomas) 3.
  • Ectopic Pregnancy Rupture: Tubal ectopic gestation leading to significant hemoperitoneum and subdiaphragmatic blood accumulation, occasionally projecting referred diaphragmatic pain to the shoulder 3.
  • Acute Peritoneal Inflammation: Subdiaphragmatic abscess formation, perforated gastric or duodenal ulcers, acute pancreatitis involving the tail of the pancreas, and perforated appendicitis with diffuse peritoneal contamination 3.

Pathophysiology

The pathogenesis of Kehr sign relies entirely on neuroanatomical convergence within the central nervous system 2,3. The muscular and peritoneal structures of the central diaphragm derive their primary sensory and motor innervation from the phrenic nerve, formed by nerve roots originating from the third, fourth, and fifth cervical spinal segments (C3-C5). When blood, digestive enzymes, or purulent exudate accumulates within the peritoneal cavity, gravity and patient positioning direct fluid toward the subdiaphragmatic space, particularly when the patient is supine or in a Trendelenburg position. This fluid directly contacts and irritates the peritoneal mesothelium overlying the inferior surface of the diaphragm 2,3. Nociceptive impulses generated by this irritation travel centrally along the afferent fibers of the phrenic nerve, entering the cervical spinal cord at the C3-C5 levels. Within the dorsal horn of the cervical spinal cord, these visceral afferent fibers converge upon the same second-order projection neurons that receive somatic sensory inputs from the cutaneous dermatomes of the left shoulder and supraclavicular region (supplied by the supraclavicular nerves, also arising from C3 and C4). The cerebral cortex fails to distinguish the precise origin of the incoming electrical signal, erroneously localizing the nociceptive sensation to the somatic dermatome rather than the visceral source—a classic clinical manifestation of referred visceral pain 2,3. Furthermore, active contraction of the diaphragm during deep inspiration depresses the dome of the muscle further against the subdiaphragmatic fluid collection, stretching the irritated peritoneal lining and sharply exacerbating the referred shoulder pain.

Kehr sign — Pathophysiological Cascade & Clinical Flowchart 1 Intraperitoneal Pathology Hemoperitoneum, splenic rupture, or subdiaphragmatic blood accumulation irritating the peritoneal lining 2 Neural Convergence Irritation of the peritoneal surface of the diaphragm, which shares common sensory innervation with the shoulder via the phrenic nerve 3 Spinal Projection Afferent C3-C5 nerve fibers enter the cervical spinal cord, converging with somatic sensory fibers originating from the left shoulder dermatomes 4 Cortical Misinterpretation The cerebral cortex misinterprets visceral diaphragmatic nociceptive input as somatic pain originating from the left shoulder tip 5 Therapeutic Intervention Prompt diagnostic imaging, aggressive fluid resuscitation, and urgent surgical intervention to mitigate hemorrhagic shock

Clinical Presentation & Classic Clinical Signs

  • History & Cardinal Symptoms: Patients typically report the acute onset of sharp, constant, or pleuritic pain localized to the left shoulder tip or supraclavicular fossa, accompanied by left upper quadrant or generalized abdominal pain 2,3. Nausea, early satiety, generalized abdominal bloating, dizziness, lightheadedness, and syncope may develop as intravascular volume depletion progresses 3.
  • Physical Examination & Named Clinical Signs:
    • Kehr Sign: Elicitation or spontaneous worsening of left shoulder pain upon deep inspiration or when pressure is applied to the left upper quadrant of the abdomen 2,3.
    • Balance Sign: Fixed dullness to percussion in the left flank and shifting dullness in the right flank, indicating localized clot formation around the spleen alongside freely flowing intraperitoneal blood 3.
    • Ballance's Sign: Diminished or absent bowel sounds associated with paralytic ileus secondary to peritoneal irritation 3.
    • Cullen Sign & Grey Turner Sign: Periumbilical or flank ecchymosis occasionally observed in delayed presentations of massive hemoperitoneum or retroperitoneal hemorrhage 3.
    • Hemodynamic Instability: Tachycardia, tachypnea, narrow pulse pressure, delayed capillary refill, and profound orthostatic hypotension indicative of Class III or IV hemorrhagic shock 3.

Diagnostic Workup & Interpretation (Laboratory, Imaging & ECG/Pathology)

Diagnostic Modality / Test Expected Clinical & Radiological / Laboratory Finding
Gold-Standard InvestigationContrast-enhanced computed tomography (CE-CT) of the abdomen and pelvis demonstrating high-attenuation free fluid (blood) in the perihepatic, perisplenic, and pelvic gutters, coupled with parenchymal splenic laceration, subcapsular hematoma, or active contrast extravasation ("sentinel clot sign").
Laboratory PanelComplete blood count reveals progressive normocytic anemia (falling hemoglobin and hematocrit), initial reactive leukocytosis (white blood cell count greater than 12,000 to 15,000 /mcL due to stress response or underlying infection), elevated serum lactate, and baseline coagulopathy (prolonged PT/INR and aPTT).
Imaging / Radiology (X-ray, US, CT, MRI)Focused Assessment with Sonography for Trauma (FAST) exam identifies free fluid in Morison's pouch, the splenorenal recess, and the pouch of Douglas. Plain chest and abdominal radiographs may demonstrate elevated left hemidiaphragm, obliteration of the splenic shadow, left basilar atelectasis, and medial displacement of the gastric bubble.
ECG / Histopathology / Procedural12-lead electrocardiogram performed routinely to exclude acute coronary syndrome or inferior/posterior myocardial ischemia as a differential source of referred shoulder or chest pain. Diagnostic peritoneal aspiration (DPA) or diagnostic peritoneal lavage (DPL) confirms frank, non-clotting blood in unstable trauma patients when CT is unavailable.

Staging, Classification & Clinical Scoring Systems

Criterion / Stage / Score Component Clinical Threshold, Points & Management Implication
American Association for the Surgery of Trauma (AAST) Organ Injury Scale: Grade ISubcapsular hematoma spanning less than 10 percent of surface area; capsular tear less than 1 centimeter in parenchymal depth. Managed non-operatively with close hemodynamic monitoring in stable patients.
AAST Organ Injury Scale: Grade IISubcapsular hematoma involving 10 to 50 percent of surface area; laceration 1 to 3 centimeters in parenchymal depth involving no major trabecular vessels. Conservative observation or angioembolization.
AAST Organ Injury Scale: Grade IIISubcapsular hematoma exceeding 50 percent of surface area or expanding; ruptured subcapsular or parenchymal hematoma; laceration greater than 3 centimeters in depth or involving trabecular vessels. Close monitoring versus angioembolization or surgical repair.
AAST Organ Injury Scale: Grade IV & VGrade IV: Laceration involving segmental or hilar vessels producing major devascularization (greater than 25 percent of spleen). Grade V: Completely shattered spleen or hilar vascular injury with total devascularization. Immediate surgical intervention (splenectomy or urgent partial splenectomy) required.

Differential Diagnosis

Differential Condition Distinguishing Clinical, Biochemical & Imaging Features
Acute Myocardial Infarction / PericarditisPresents with chest discomfort radiating to the left shoulder or jaw, associated with characteristic ST-segment elevations or depressions on ECG and elevated cardiac troponin levels; lacks localized abdominal tenderness or peritoneal signs.
Acute Pleuritis / Pneumonia / Pulmonary EmbolismCharacterized by pleuritic chest pain, dyspnea, and cough; chest radiography or CT pulmonary angiogram reveals pulmonary infiltrates, pleural effusion, or filling defects in pulmonary arteries without hemoperitoneum.
Subdiaphragmatic AbscessAccompanied by persistent high-grade fevers, leukocytosis, recent abdominal surgery or intra-abdominal sepsis; cross-sectional imaging demonstrates a localized loculated fluid collection with peripheral enhancement beneath the diaphragm.
Intrinsic Shoulder Pathology (Rotator Cuff Tendinopathy / Bursitis)Shoulder pain is strictly localized, mechanically induced by active or passive range of motion of the glenohumeral joint, and completely independent of respiration, abdominal palpation, or intra-abdominal pathology.

Management & Treatment Protocol

  • Initial Stabilization & Resuscitation: Establish two large-bore peripheral intravenous lines (16-gauge or larger) or a central venous catheter. Initiate aggressive fluid resuscitation using weight-based warm isotonic crystalloids (e.g., 20 mL/kg bolus of Plasmalyte or Lactated Ringer's solution). Draw blood immediately for type and crossmatch, complete blood count, coagulation profile, and arterial blood gases. Initiate MTP (Massive Transfusion Protocol) with uncrossmatched O-negative blood or type-specific blood products if hemodynamic instability persists 3.
  • First-Line Medical / Pharmacological Therapy (with exact adult dosing):
    • Analgesia: IV administration of Morphine sulfate (2 to 4 mg IV every 3 to 4 hours PRN) or Fentanyl (50 to 100 mcg IV every 1 to 2 hours PRN) for acute somatic and referred pain titration.
    • Antiemetic Therapy: Ondansetron 4 mg IV every 8 hours PRN to control nausea and prevent vagal-mediated emesis.
    • Antimicrobial Prophylaxis: In cases of suspected hollow viscus perforation or post-procedural sepsis, administer Piperacillin-tazobactam 3.375 g IV every 6 hours or Cefoxitin 2 g IV every 6 hours. Post-splenectomy patients require mandatory vaccination against encapsulated organisms (Streptococcus pneumoniae, Neisseria meningitidis, and Haemophilus influenzae type b) administered at least 14 days post-operatively or prior to discharge.
    • - Surgical / Interventional Indications:
    • Urgent Exploratory Laparotomy / Splenectomy: Indicated for hemodynamically unstable patients (persistent systolic blood pressure less than 90 mmHg despite fluid resuscitation), active contrast extravasation on CT, high-grade splenic injuries (AAST Grades IV-V), or peritonitis. Total splenectomy or spleen-preserving partial resection is performed depending on the extent of parenchymal disruption 2,3.
    • Transcatheter Arterial Embolization (TAE): Performed by interventional radiology in hemodynamically stable patients exhibiting high-grade splenic injuries with active pseudoaneurysm formation or vascular blush to preserve splenic immunological function.

Complications & Prognosis

  • Acute Hemorrhagic Shock: Severe hypovolemia leading to multiorgan dysfunction syndrome, acute tubular necrosis, and cardiac arrest if surgical hemostasis is delayed 3.
  • Overwhelming Post-Splenectomy Infection (OPSI): A life-threatening, rapidly progressive sepsis syndrome caused by encapsulated bacterial pathogens (most notably Streptococcus pneumoniae), carrying a high mortality rate even with aggressive antibiotic therapy.
  • Thromboembolic Complications: Reactive thrombocytosis following splenectomy can precipitate portal vein thrombosis, mesenteric vein thrombosis, or deep venous thrombosis, requiring prophylactic low-molecular-weight heparin (e.g., Enoxaparin 40 mg subcutaneously once daily) when bleeding risks subside.
  • Prognosis: Overall mortality and morbidity rates depend directly on the rapidity of diagnosis, the volume of blood loss, and associated injuries. Modern management protocols yield excellent survival outcomes for isolated splenic trauma and associated Kehr sign presentation, though diagnostic delays in occult spontaneous ruptures historically carry significant mortality risks 2,3.