[Academic Presentation] Diagnosis and Treatment of Severe Abdominal-Type Henoch–Schönlein Purpura: A Case Report

Patient, male, 14 years old. He has had petechiae and ecchymoses on both lower limbs for half a month, with worsening symptoms and abdominal pain for the past 10 days. About two weeks ago, following a cold, he developed swelling and pain in the lower extremities, which gradually progressed to scattered petechiae and ecchymoses on both legs. Ten days ago, he began experiencing episodic abdominal pain. At a local hospital, he was diagnosed with “allergic purpura” and treated with intravenous vitamin C, omeprazole, and oral Yangxueyin liquid; these interventions led to some relief of the lower‑extremity rash, ecchymoses, swelling, and pain, but his abdominal pain persisted, accompanied by nausea and vomiting, intermittent rectal bleeding, and marked nocturnal abdominal discomfort. Since onset, the patient has reported fatigue, poor appetite, normal urination, no fever, and no significant weight change. He was admitted to the outpatient clinic with a diagnosis of allergic purpura (abdominal type). On admission, his vital signs were stable; the abdomen was soft with no tenderness. Scattered petechiae and ecchymoses of varying sizes were noted on all four limbs, more prominent on the lower extremities; large, pale purple ecchymoses were observed on the dorsum of the feet and hands. There was no joint swelling or tenderness. Blood tests showed WBC 18.38 × 10^9/L, platelets 186 × 10^9/L, neutrophils 0.933, and Hb 108 g/L. Fecal occult blood was positive. An upright abdominal radiograph revealed gas distension along the colon and in the left upper quadrant, with a small fluid–air level in the left upper abdomen. Given the clear cutaneous findings, combined with significant abdominal pain and gastrointestinal bleeding, the admitting diagnosis was considered severe abdominal-type allergic purpura. The patient was placed NPO, and treatment was initiated with methylprednisolone 40 mg/day IV, supplemented by gastroprotective agents, anisodamine, and atropine to alleviate abdominal pain. The next day, the patient suddenly developed severe abdominal pain, unable to lie still. Physical examination revealed: temperature 35.8°C, pulse 140 beats/min, respiration 25 breaths/min, blood pressure 110/65 mmHg. The abdomen was soft with no palpable tenderness or rebound tenderness, and the abdominal wall was relaxed without muscle guarding. Intravenous omeprazole sodium 40 mg failed to provide relief; a venous access was established, esomeprazole sodium 40 mg was infused, and a consultation with the Department of Gastroenterology was urgently requested. Despite these measures, the abdominal pain persisted, accompanied by agitation. Under cardiac monitoring, promethazine 25 mg and vitamin K3 4 mg were administered intramuscularly, and, in accordance with the gastroenterology team’s recommendations, gastrointestinal decompression, intermittent low‑flow oxygen therapy, and NPO status were instituted. Thirty minutes later, the abdominal pain remained severe; another intramuscular injection of promethazine 25 mg and one unit of thrombin were given, but neither analgesia nor hemostasis proved effective. The patient remained alert but increasingly agitated; pulse rate reached 170 beats/min. Intramuscular anisodamine 10 mg provided no relief, and benzobarbital sodium 50 mg was added intravenously. Subsequently, chlorpromazine 25 mg and promethazine 25 mg were administered intramuscularly. Despite these interventions, the patient continued to suffer from severe abdominal pain, with episodes of delirium and agitation. Following a reassessment of his condition, pethidine hydrochloride 50 mg was administered intramuscularly; five minutes later, the patient became calmer, and his vital signs gradually stabilized before he fell asleep. Considering the severity of the gastrointestinal symptoms and the unsuitability of high‑dose corticosteroid therapy, fresh frozen plasma 200–220 mL and human immunoglobulin 15–20 g were infused intravenously. The patient’s clinical course and mental state improved markedly; the rash on both lower limbs largely resolved, though recurrent abdominal pain and lower gastrointestinal bleeding persisted, managed symptomatically.

On the morning of the seventh day after admission, the patient again developed marked abdominal pain accompanied by frequent vomiting. Despite intramuscular administration of metoclopramide 10 mg and promethazine 50 mg, along with oral esomeprazole enteric‑coated tablets 40 mg, there was no relief. Following the addition of granisetron hydrochloride injection 3 mg administered intravenously, the vomiting subsided; however, the patient became agitated. Under continuous cardiac monitoring and supplemental oxygen, the patient received an intramuscular injection of pethidine hydrochloride 50 mg and an intravenous push of diazepam 5 mg, after which the patient’s mood gradually stabilized and the abdominal pain improved. Half an hour later, 100 mL of bloody watery stool was passed. Urgent abdominal ultrasound revealed intestinal wall thickening measuring 0.8 cm, with nearly absent peristalsis, a small amount of free fluid in the peritoneal cavity, and no definite mass in the right lower quadrant at the appendiceal region. Abdominal CT showed dilated bowel loops with pneumatosis, and air–fluid levels were observed in some segments. Given that the patient’s predominant symptoms at this time were gastrointestinal and the possibility of intestinal ischemia, necrosis, or perforation could not be ruled out, a consultation with the Department of Gastroenterology was sought, and the patient was subsequently transferred to that department for further management.

After transfer to the Department of Gastroenterology, the patient continued to experience intermittent abdominal pain, without vomiting or hematochezia, and with diminished bowel sounds. Repeat complete blood count showed a white blood cell count of 12.86 × 10^9/L and a neutrophil percentage of 66.1%. Colonoscopy and dual-source abdominal CT revealed no obvious organic intestinal lesions. The final diagnosis was lower gastrointestinal bleeding and allergic purpura (abdominal type) with incomplete intestinal obstruction. Further management included strict NPO status; in addition to continuing methylprednisolone 40 mg/day to control the underlying condition, acid suppression, hemostasis, spasmolysis, and nutritional support were intensified. Subsequently, the patient’s abdominal pain and gastrointestinal bleeding gradually improved, and they were discharged in stable condition.

Henoch–Schönlein purpura (HSP) is a leukocytoclastic vasculitis mediated by IgA immune complexes, affecting capillaries and small arterioles. It may involve the skin, joints, gastrointestinal tract, and kidneys. The classic clinical presentation includes an acute onset of palpable cutaneous purpura, arthralgia with swelling, and abdominal pain. Renal involvement typically manifests as microscopic hematuria and trace proteinuria. HSP most commonly affects children aged 2 to 10 years, though adults can also be affected. Up to 75% of patients develop gastrointestinal symptoms, known as abdominal-type HSP, which may occur concurrently with or precede cutaneous manifestations. Common gastrointestinal signs include abdominal pain and vomiting; in severe cases, mucosal congestion and edema can lead to paroxysmal, intense abdominal pain and gastrointestinal bleeding. In rare instances, more serious complications such as intussusception or intestinal perforation may arise, along with pancreatitis, gallbladder hydrops, and… Complications such as protein‑losing enteropathy. In abdominal‑type HSP, gastrointestinal symptoms are often recurrent, the disease course is prolonged, and treatment is challenging.

The etiology and pathogenesis of HSP remain incompletely elucidated; current evidence suggests that its onset may be associated with factors such as infection, vaccination, food and drug exposure, and genetics. The primary pathogenic mechanism involves dysregulated IgA‑mediated humoral immunity, with IgA deposition in small vessel walls triggering autoinflammatory responses and tissue injury that play a pivotal role in the development of HSP. In the gastrointestinal tract, vasculitis leads to mucosal and serosal hemorrhage, edema, and erosions; submucosal vascular wall necrosis, intestinal wall edema, necrosis, and ulceration; increased vascular permeability and fragility; and ischemic damage to gastrointestinal smooth muscle, resulting in motility disturbances. The abdominal form of HSP is characterized primarily by abdominal pain, which is often migratory, frequently localized around the umbilicus, in the lower abdomen, or throughout the abdomen. It typically presents as sudden, severe colicky pain in the periumbilical or lower abdominal region, occurring in paroxysms that may progressively worsen, with or without accompanying vomiting. Physical signs, however, are minimal: tenderness is often poorly localized, with only mild palpation pain, and marked abdominal muscle guarding or rebound tenderness is usually absent. This dissociation between symptoms and physical findings is a key clinical feature distinguishing the abdominal form of HSP from acute abdominal conditions. Laboratory studies may reveal normal or mildly elevated white blood cell counts. Clinically, the abdominal form… Abdominal symptoms in HSP often occur concurrently with purpuric manifestations and may, on occasion, precede them; therefore, prior to initiating treatment, it is essential to clearly determine the nature of the patient’s abdominal pain and gastrointestinal bleeding and to promptly perform imaging studies such as upright abdominal radiographs, ultrasound, and CT scans to prevent misdiagnosis. In this case, the skin findings were typical palpable cutaneous purpura, while the gastrointestinal symptoms included recurrent severe abdominal pain and hematochezia, without marked rebound tenderness or muscle rigidity, indicating a severe abdominal‑type presentation of HSP.

Regarding the treatment of severe abdominal-type HSP, clinical studies reported abroad have demonstrated that systemic glucocorticoid therapy can effectively alleviate joint pain and abdominal pain associated with Henoch–Schönlein purpura and shorten the duration of skin lesions. The 2013 Evidence-Based Guidelines for the Diagnosis and Treatment of Pediatric Henoch–Schönlein Purpura issued by the Chinese Medical Association recommend early corticosteroid use in children with severe abdominal symptoms; however, no consensus exists regarding specific dosing or treatment duration. In my clinical experience, corticosteroids should be initiated promptly, with the dose tailored to the severity of gastrointestinal symptoms. For mild, intermittent abdominal pain, an adequate initial dose can rapidly control the condition and prevent progression to a more severe form. Conversely, when abdominal pain is frequent, severe, and accompanied by overt gastrointestinal bleeding, the initial corticosteroid dose should be modest, and the dose should not be escalated prematurely if symptom improvement remains inadequate. Intravenous plasma exchange and intravenous immunoglobulin may be considered to attenuate immune‑inflammatory responses and thereby mitigate the severe gastrointestinal vasculitis caused by HSP. Concurrently, early fasting and gastrointestinal decompression are essential, along with timely administration of proton pump inhibitors such as omeprazole sodium or esomeprazole sodium and gastroprotective agents to reduce gastric acid secretion, safeguard the gastrointestinal mucosa, decrease mucosal edema and hemorrhage, and promote mucosal healing—thus enhancing the safety of corticosteroid therapy. When sudden abdominal pain occurs, while ruling out acute abdominal conditions, spasmolytics, analgesics, sedatives, and hemostatics should be administered as indicated; commonly used agents include scopolamine, atropine, promethazine, and phenobarbital sodium. Special attention should also be paid to psychiatric manifestations—such as agitation, anxiety, or fear—that may accompany severe abdominal pain, as well as drug‑induced delirium, and medications should be selected judiciously. Notably, patient–physician communication is particularly critical in managing severe abdominal‑type HSP. For patients presenting with abdominal pain, it is important to promptly educate both the patient and family about the significance of dietary restrictions, including semi‑liquid diets and fasting, while closely monitoring bowel movements and flatus. In cases of sudden onset of abdominal pain, timely communication with the patient and family is essential to prevent anxiety and fear related to pain and bleeding, which could otherwise compromise clinical judgment and medication management.

Thus, for the treatment of severe abdominal‑type HSP, early administration of adequate doses of glucocorticoids is critical; when high‑dose corticosteroids are poorly tolerated, plasma exchange and intravenous immunoglobulin may be added to mitigate vasculitic manifestations. The combined use of proton pump inhibitors and gastric mucosal protectants provides a safety foundation for corticosteroid therapy and serves as an important measure to alleviate mucosal edema and bleeding. Early gastrointestinal decompression, appropriate symptomatic management, and thorough communication regarding the patient’s condition are key factors influencing both the clinical course and prognosis of severe abdominal‑type HSP.