The Clinical Picture

A 53-year-old man presented with acute altered mental status secondary to methamphetamine intoxication. On hospital day 2, he developed macular, violaceous skin lesions with interconnecting rings on his abdomen and back, consistent with livedo reticularis (Figure 1). The extensive distribution of the lesions on the abdomen raised concern for underlying disease.

Livedo reticularis can be the manifestation of a wide range of conditions: hematologic and hypercoagulable states, embolic events, connective tissue disease, infection, vasculitis, malignancy, neurologic and endocrine conditions, and medication effects.¹ Our patient had no recent history of vascular procedures or peripheral eosinophilia to suggest cholesterol embolization, and he had not recently started taking any new medications. His current medications included aspirin 81 mg, atorvastatin 40 mg, amlodipine 10 mg, and insulin glargine 20 units. Tests for cryoglobulin and antiphospholipid antibodies were negative. There was no evidence of malignancy, and evaluations for infectious and autoimmune diseases were negative.

Biopsy study of a skin lesion showed features consistent with livedo reticularis, with no evidence of vasculitis. The lesions resolved without definitive therapy by hospital day 3. This, in addition to other features of the lesions (eg, uniformity, unbroken reticular segments) and the extensive negative workup for systemic disease, suggested primary livedo reticularis.

CAUSES, TYPES, SUBTYPES

Livedo reticularis results from changes in the cutaneous microvasculature, composed of central arterioles that drain into an interconnecting, netlike venous plexus.^1,2 Conditions such as arteriolar deoxygenation and venous plexus venodilation­ that result in a prominent venous plexus can give rise to clinical livedo reticularis.³

Adapted from information in References 1 and 4.

Livedo reticularis is divided into 2 broad categories depending on whether it is associated with systemic disease or not (Figure 2).^3,4 In the absence of systemic symptoms, it can be further divided into 3 subcategories: idiopathic, physiologic, and primary.¹ It is considered idiopathic if it is persistent, whereas physiologic and primary forms have a fluctuating course.⁴ Physiologic livedo reticularis often occurs in the periphery due to exposure to cold temperatures that cause vasospasm that resolves in warm temperatures.

Primary livedo reticularis is thought to occur from spontaneous arteriolar vasospasm. It is a diagnosis of exclusion. An evaluation for underlying disease is important, as livedo reticularis can be associated with the range of conditions listed above.

In our patient, methamphetamine was considered a possible cause, but the findings of livedo reticularis were delayed and persisted longer than expected if they were drug-related.

Livedo racemosa

Distinguishing livedo reticularis from livedo racemosa is important. Livedo racemosa is always secondary and is often associated with antiphospholipid syndrome. It is present in 25% of cases of primary antiphospholipid syndrome and in up to 70% of cases of antiphospholipid syndrome associated with systemic lupus erythematosus.⁵ The reticular pattern of livedo racemosa is permanent and often has irregular and incomplete segments of reticular lattice, with a distribution that is more generalized,  involving the trunk or buttocks (or both) in addition to the extremities.^3,4 Consequently, a thorough history and physical examination are needed to guide additional workup.

A 53-year-old man presented with acute altered mental status secondary to methamphetamine intoxication. On hospital day 2, he developed macular, violaceous skin lesions with interconnecting rings on his abdomen and back, consistent with livedo reticularis (Figure 1). The extensive distribution of the lesions on the abdomen raised concern for underlying disease.

Livedo reticularis can be the manifestation of a wide range of conditions: hematologic and hypercoagulable states, embolic events, connective tissue disease, infection, vasculitis, malignancy, neurologic and endocrine conditions, and medication effects.¹ Our patient had no recent history of vascular procedures or peripheral eosinophilia to suggest cholesterol embolization, and he had not recently started taking any new medications. His current medications included aspirin 81 mg, atorvastatin 40 mg, amlodipine 10 mg, and insulin glargine 20 units. Tests for cryoglobulin and antiphospholipid antibodies were negative. There was no evidence of malignancy, and evaluations for infectious and autoimmune diseases were negative.

Biopsy study of a skin lesion showed features consistent with livedo reticularis, with no evidence of vasculitis. The lesions resolved without definitive therapy by hospital day 3. This, in addition to other features of the lesions (eg, uniformity, unbroken reticular segments) and the extensive negative workup for systemic disease, suggested primary livedo reticularis.

CAUSES, TYPES, SUBTYPES

Livedo reticularis results from changes in the cutaneous microvasculature, composed of central arterioles that drain into an interconnecting, netlike venous plexus.^1,2 Conditions such as arteriolar deoxygenation and venous plexus venodilation­ that result in a prominent venous plexus can give rise to clinical livedo reticularis.³

Adapted from information in References 1 and 4.

Livedo reticularis is divided into 2 broad categories depending on whether it is associated with systemic disease or not (Figure 2).^3,4 In the absence of systemic symptoms, it can be further divided into 3 subcategories: idiopathic, physiologic, and primary.¹ It is considered idiopathic if it is persistent, whereas physiologic and primary forms have a fluctuating course.⁴ Physiologic livedo reticularis often occurs in the periphery due to exposure to cold temperatures that cause vasospasm that resolves in warm temperatures.

Primary livedo reticularis is thought to occur from spontaneous arteriolar vasospasm. It is a diagnosis of exclusion. An evaluation for underlying disease is important, as livedo reticularis can be associated with the range of conditions listed above.

In our patient, methamphetamine was considered a possible cause, but the findings of livedo reticularis were delayed and persisted longer than expected if they were drug-related.

Livedo racemosa

Distinguishing livedo reticularis from livedo racemosa is important. Livedo racemosa is always secondary and is often associated with antiphospholipid syndrome. It is present in 25% of cases of primary antiphospholipid syndrome and in up to 70% of cases of antiphospholipid syndrome associated with systemic lupus erythematosus.⁵ The reticular pattern of livedo racemosa is permanent and often has irregular and incomplete segments of reticular lattice, with a distribution that is more generalized,  involving the trunk or buttocks (or both) in addition to the extremities.^3,4 Consequently, a thorough history and physical examination are needed to guide additional workup.

A 53-year-old man presented with acute altered mental status secondary to methamphetamine intoxication. On hospital day 2, he developed macular, violaceous skin lesions with interconnecting rings on his abdomen and back, consistent with livedo reticularis (Figure 1). The extensive distribution of the lesions on the abdomen raised concern for underlying disease.

Livedo reticularis can be the manifestation of a wide range of conditions: hematologic and hypercoagulable states, embolic events, connective tissue disease, infection, vasculitis, malignancy, neurologic and endocrine conditions, and medication effects.¹ Our patient had no recent history of vascular procedures or peripheral eosinophilia to suggest cholesterol embolization, and he had not recently started taking any new medications. His current medications included aspirin 81 mg, atorvastatin 40 mg, amlodipine 10 mg, and insulin glargine 20 units. Tests for cryoglobulin and antiphospholipid antibodies were negative. There was no evidence of malignancy, and evaluations for infectious and autoimmune diseases were negative.

Biopsy study of a skin lesion showed features consistent with livedo reticularis, with no evidence of vasculitis. The lesions resolved without definitive therapy by hospital day 3. This, in addition to other features of the lesions (eg, uniformity, unbroken reticular segments) and the extensive negative workup for systemic disease, suggested primary livedo reticularis.

CAUSES, TYPES, SUBTYPES

Livedo reticularis results from changes in the cutaneous microvasculature, composed of central arterioles that drain into an interconnecting, netlike venous plexus.^1,2 Conditions such as arteriolar deoxygenation and venous plexus venodilation­ that result in a prominent venous plexus can give rise to clinical livedo reticularis.³

Adapted from information in References 1 and 4.

Livedo reticularis is divided into 2 broad categories depending on whether it is associated with systemic disease or not (Figure 2).^3,4 In the absence of systemic symptoms, it can be further divided into 3 subcategories: idiopathic, physiologic, and primary.¹ It is considered idiopathic if it is persistent, whereas physiologic and primary forms have a fluctuating course.⁴ Physiologic livedo reticularis often occurs in the periphery due to exposure to cold temperatures that cause vasospasm that resolves in warm temperatures.

Primary livedo reticularis is thought to occur from spontaneous arteriolar vasospasm. It is a diagnosis of exclusion. An evaluation for underlying disease is important, as livedo reticularis can be associated with the range of conditions listed above.

In our patient, methamphetamine was considered a possible cause, but the findings of livedo reticularis were delayed and persisted longer than expected if they were drug-related.

Livedo racemosa

Distinguishing livedo reticularis from livedo racemosa is important. Livedo racemosa is always secondary and is often associated with antiphospholipid syndrome. It is present in 25% of cases of primary antiphospholipid syndrome and in up to 70% of cases of antiphospholipid syndrome associated with systemic lupus erythematosus.⁵ The reticular pattern of livedo racemosa is permanent and often has irregular and incomplete segments of reticular lattice, with a distribution that is more generalized,  involving the trunk or buttocks (or both) in addition to the extremities.^3,4 Consequently, a thorough history and physical examination are needed to guide additional workup.

A  44-year-old woman was admitted to the  hospital for the second time in 2 months with acute onset of severe abdominal pain. She had a history of cervical cancer treated with total hysterectomy with bilateral salpingo-oophorectomy, chemotherapy, and radiotherapy at age 38.

Abdominal examination revealed shifting dullness and tenderness without guarding. Massive ascites and irregularity in the bladder wall were detected on ultrasonography and follow-up computed tomography (Figure 1). Ascitic fluid collected during the previous admission had shown an elevated ascitic fluid-serum creatinine ratio (4.37) (reference range ≤ 1.0), highly suggestive of intraperitoneal urine leakage.¹ Thus, ascites was assumed to represent intraperitoneal urine leakage due to bladder rupture.

Cystoscopy revealed thinning of the bladder wall with a fistula, and cystography confirmed intraperitoneal leakage of contrast medium from the bladder (Figure 2). This led to the diagnosis of urinary ascites from spontaneous bladder rupture following radiation therapy for cervical cancer. She chose conservative treatment (night-time urinary catheterization without surgery), as the bladder wall was diffusely thinned, making surgery difficult. Outpatient follow-up was uneventful.

LONG-TERM EFFECTS OF RADIATION ON THE BLADDER

Urinary ascites from intraperitoneal urine leakage is a rare but clinically important sequel to bladder fistula or bladder wall rupture. Fistula or rupture can be caused by pelvic irradiation, blunt trauma, or surgical procedures, but may also be spontaneous.²

When the total radiation dose to the bladder exceeds 60 Gy, radiation cystitis may occur, leading to bladder fistula.³ Effects of radiation on the bladder are usually seen within 2 to 4 years³ but may occur long after the completion of radiation therapy—10 years² or even 30 to 40 years later.⁴ Therefore, ascites of unknown origin in a patient with a history of pelvic radiation therapy should lead to an evaluation for late radiation cystitis and urinary ascites from bladder rupture.

A  44-year-old woman was admitted to the  hospital for the second time in 2 months with acute onset of severe abdominal pain. She had a history of cervical cancer treated with total hysterectomy with bilateral salpingo-oophorectomy, chemotherapy, and radiotherapy at age 38.

Abdominal examination revealed shifting dullness and tenderness without guarding. Massive ascites and irregularity in the bladder wall were detected on ultrasonography and follow-up computed tomography (Figure 1). Ascitic fluid collected during the previous admission had shown an elevated ascitic fluid-serum creatinine ratio (4.37) (reference range ≤ 1.0), highly suggestive of intraperitoneal urine leakage.¹ Thus, ascites was assumed to represent intraperitoneal urine leakage due to bladder rupture.

Cystoscopy revealed thinning of the bladder wall with a fistula, and cystography confirmed intraperitoneal leakage of contrast medium from the bladder (Figure 2). This led to the diagnosis of urinary ascites from spontaneous bladder rupture following radiation therapy for cervical cancer. She chose conservative treatment (night-time urinary catheterization without surgery), as the bladder wall was diffusely thinned, making surgery difficult. Outpatient follow-up was uneventful.

LONG-TERM EFFECTS OF RADIATION ON THE BLADDER

Urinary ascites from intraperitoneal urine leakage is a rare but clinically important sequel to bladder fistula or bladder wall rupture. Fistula or rupture can be caused by pelvic irradiation, blunt trauma, or surgical procedures, but may also be spontaneous.²

When the total radiation dose to the bladder exceeds 60 Gy, radiation cystitis may occur, leading to bladder fistula.³ Effects of radiation on the bladder are usually seen within 2 to 4 years³ but may occur long after the completion of radiation therapy—10 years² or even 30 to 40 years later.⁴ Therefore, ascites of unknown origin in a patient with a history of pelvic radiation therapy should lead to an evaluation for late radiation cystitis and urinary ascites from bladder rupture.

A  44-year-old woman was admitted to the  hospital for the second time in 2 months with acute onset of severe abdominal pain. She had a history of cervical cancer treated with total hysterectomy with bilateral salpingo-oophorectomy, chemotherapy, and radiotherapy at age 38.

Abdominal examination revealed shifting dullness and tenderness without guarding. Massive ascites and irregularity in the bladder wall were detected on ultrasonography and follow-up computed tomography (Figure 1). Ascitic fluid collected during the previous admission had shown an elevated ascitic fluid-serum creatinine ratio (4.37) (reference range ≤ 1.0), highly suggestive of intraperitoneal urine leakage.¹ Thus, ascites was assumed to represent intraperitoneal urine leakage due to bladder rupture.

Cystoscopy revealed thinning of the bladder wall with a fistula, and cystography confirmed intraperitoneal leakage of contrast medium from the bladder (Figure 2). This led to the diagnosis of urinary ascites from spontaneous bladder rupture following radiation therapy for cervical cancer. She chose conservative treatment (night-time urinary catheterization without surgery), as the bladder wall was diffusely thinned, making surgery difficult. Outpatient follow-up was uneventful.

LONG-TERM EFFECTS OF RADIATION ON THE BLADDER

Urinary ascites from intraperitoneal urine leakage is a rare but clinically important sequel to bladder fistula or bladder wall rupture. Fistula or rupture can be caused by pelvic irradiation, blunt trauma, or surgical procedures, but may also be spontaneous.²

When the total radiation dose to the bladder exceeds 60 Gy, radiation cystitis may occur, leading to bladder fistula.³ Effects of radiation on the bladder are usually seen within 2 to 4 years³ but may occur long after the completion of radiation therapy—10 years² or even 30 to 40 years later.⁴ Therefore, ascites of unknown origin in a patient with a history of pelvic radiation therapy should lead to an evaluation for late radiation cystitis and urinary ascites from bladder rupture.

A 45-year-old man with known human immunodeficiency virus infection presented with a 5-day history of dyspnea. When his dyspnea had become symptomatic, he had restarted his home dapsone prophylaxis, but his dyspnea had progressively worsened, and his urine became dark.

On presentation to our institution, he was tachycardic, tachypneic, hypoxic, and cyanotic (Figure 1). Chest radiography revealed multifocal bilateral airspace opacities. He was started on vancomycin and piperacillin-tazobactam for treatment of presumed pneumonia, and his dapsone was continued for prophylaxis against Pneumocystis jirovecii pneumonia.

During the next several hours, his hypoxia worsened, and his peripheral capillary oxygen saturation was 87% despite use of a Venturi mask at a 35% fraction of inspired oxygen. Arterial blood gas testing revealed an elevated partial pressure of oxygen (143 mm Hg) and chocolate-brown colored arterial blood. Due to the low peripheral capillary oxygen saturation, high partial pressure of oxygen, and abnormal color of his blood (Figure 2), serum methemoglobin testing was ordered and revealed a concentration of 22.9% (normal value < 1.5%).

Based on these test results, the patient’s dapsone was stopped and replaced with atovaquone. Intravenous infusion of methylene blue was started, with subsequent improvement of the hypoxia and cyanosis (Figure 1). His urine became green, but it returned to a normal color in a matter of hours. He was ultimately diagnosed with P jirovecii pneumonia and completed a course of atovaquone with total resolution of his symptoms.

THE MECHANISMS BEHIND METHEMOGLOBINEMIA

Heme iron is normally in the ferrous state (Fe²⁺), which allows for hemoglobin to carry oxygen and release it to tissues.¹ Exposure to an oxidative stress can lead to methemoglobinemia from an increase in abnormal hemoglobin that contains iron in a ferric state (Fe³⁺).^1,2

Methemoglobin reduces oxygen-carrying capacity in two ways: it is unable to carry oxygen, and its presence shifts the oxy­gen dissociation curve to the left, causing any remaining normal hemoglobin to be unable to release oxygen to the tissues.^1,2

Causes of acquired methemoglobinemia include topical anesthetics (eg, benzocaine, lidocaine) and antibiotics (eg, dapsone).^2,3 Signs and symptoms include cyanosis, headache, fatigue, dyspnea, lethargy, respiratory distress, and dark-colored urine.^1,2

MANAGEMENT

Treatment consists of intravenous methylene blue, which reduces the hemoglobin from a ferric state to a ferrous state.^1–4 Methylene blue is a water-soluble dye excreted primarily in the urine, and common side effects include dizziness, nausea, and green urine.^5–7 The blue pigments from methylene blue combine with urobilin (a yellow pigment in the urine), producing a green color.⁷ This is not pathological and requires no treatment, as the urine returns to normal color after the body fully excretes the dye.^5–7

If intravenous methylene blue fails to produce a response, other treatments to consider include hemodialysis, blood transfusion, exchange transfusion, and hyperbaric oxygen therapy.²

A 45-year-old man with known human immunodeficiency virus infection presented with a 5-day history of dyspnea. When his dyspnea had become symptomatic, he had restarted his home dapsone prophylaxis, but his dyspnea had progressively worsened, and his urine became dark.

On presentation to our institution, he was tachycardic, tachypneic, hypoxic, and cyanotic (Figure 1). Chest radiography revealed multifocal bilateral airspace opacities. He was started on vancomycin and piperacillin-tazobactam for treatment of presumed pneumonia, and his dapsone was continued for prophylaxis against Pneumocystis jirovecii pneumonia.

During the next several hours, his hypoxia worsened, and his peripheral capillary oxygen saturation was 87% despite use of a Venturi mask at a 35% fraction of inspired oxygen. Arterial blood gas testing revealed an elevated partial pressure of oxygen (143 mm Hg) and chocolate-brown colored arterial blood. Due to the low peripheral capillary oxygen saturation, high partial pressure of oxygen, and abnormal color of his blood (Figure 2), serum methemoglobin testing was ordered and revealed a concentration of 22.9% (normal value < 1.5%).

Based on these test results, the patient’s dapsone was stopped and replaced with atovaquone. Intravenous infusion of methylene blue was started, with subsequent improvement of the hypoxia and cyanosis (Figure 1). His urine became green, but it returned to a normal color in a matter of hours. He was ultimately diagnosed with P jirovecii pneumonia and completed a course of atovaquone with total resolution of his symptoms.

THE MECHANISMS BEHIND METHEMOGLOBINEMIA

Heme iron is normally in the ferrous state (Fe²⁺), which allows for hemoglobin to carry oxygen and release it to tissues.¹ Exposure to an oxidative stress can lead to methemoglobinemia from an increase in abnormal hemoglobin that contains iron in a ferric state (Fe³⁺).^1,2

Methemoglobin reduces oxygen-carrying capacity in two ways: it is unable to carry oxygen, and its presence shifts the oxy­gen dissociation curve to the left, causing any remaining normal hemoglobin to be unable to release oxygen to the tissues.^1,2

Causes of acquired methemoglobinemia include topical anesthetics (eg, benzocaine, lidocaine) and antibiotics (eg, dapsone).^2,3 Signs and symptoms include cyanosis, headache, fatigue, dyspnea, lethargy, respiratory distress, and dark-colored urine.^1,2

MANAGEMENT

Treatment consists of intravenous methylene blue, which reduces the hemoglobin from a ferric state to a ferrous state.^1–4 Methylene blue is a water-soluble dye excreted primarily in the urine, and common side effects include dizziness, nausea, and green urine.^5–7 The blue pigments from methylene blue combine with urobilin (a yellow pigment in the urine), producing a green color.⁷ This is not pathological and requires no treatment, as the urine returns to normal color after the body fully excretes the dye.^5–7

If intravenous methylene blue fails to produce a response, other treatments to consider include hemodialysis, blood transfusion, exchange transfusion, and hyperbaric oxygen therapy.²

A 45-year-old man with known human immunodeficiency virus infection presented with a 5-day history of dyspnea. When his dyspnea had become symptomatic, he had restarted his home dapsone prophylaxis, but his dyspnea had progressively worsened, and his urine became dark.

On presentation to our institution, he was tachycardic, tachypneic, hypoxic, and cyanotic (Figure 1). Chest radiography revealed multifocal bilateral airspace opacities. He was started on vancomycin and piperacillin-tazobactam for treatment of presumed pneumonia, and his dapsone was continued for prophylaxis against Pneumocystis jirovecii pneumonia.

During the next several hours, his hypoxia worsened, and his peripheral capillary oxygen saturation was 87% despite use of a Venturi mask at a 35% fraction of inspired oxygen. Arterial blood gas testing revealed an elevated partial pressure of oxygen (143 mm Hg) and chocolate-brown colored arterial blood. Due to the low peripheral capillary oxygen saturation, high partial pressure of oxygen, and abnormal color of his blood (Figure 2), serum methemoglobin testing was ordered and revealed a concentration of 22.9% (normal value < 1.5%).

Based on these test results, the patient’s dapsone was stopped and replaced with atovaquone. Intravenous infusion of methylene blue was started, with subsequent improvement of the hypoxia and cyanosis (Figure 1). His urine became green, but it returned to a normal color in a matter of hours. He was ultimately diagnosed with P jirovecii pneumonia and completed a course of atovaquone with total resolution of his symptoms.

THE MECHANISMS BEHIND METHEMOGLOBINEMIA

Heme iron is normally in the ferrous state (Fe²⁺), which allows for hemoglobin to carry oxygen and release it to tissues.¹ Exposure to an oxidative stress can lead to methemoglobinemia from an increase in abnormal hemoglobin that contains iron in a ferric state (Fe³⁺).^1,2

Methemoglobin reduces oxygen-carrying capacity in two ways: it is unable to carry oxygen, and its presence shifts the oxy­gen dissociation curve to the left, causing any remaining normal hemoglobin to be unable to release oxygen to the tissues.^1,2

Causes of acquired methemoglobinemia include topical anesthetics (eg, benzocaine, lidocaine) and antibiotics (eg, dapsone).^2,3 Signs and symptoms include cyanosis, headache, fatigue, dyspnea, lethargy, respiratory distress, and dark-colored urine.^1,2

MANAGEMENT

Treatment consists of intravenous methylene blue, which reduces the hemoglobin from a ferric state to a ferrous state.^1–4 Methylene blue is a water-soluble dye excreted primarily in the urine, and common side effects include dizziness, nausea, and green urine.^5–7 The blue pigments from methylene blue combine with urobilin (a yellow pigment in the urine), producing a green color.⁷ This is not pathological and requires no treatment, as the urine returns to normal color after the body fully excretes the dye.^5–7

If intravenous methylene blue fails to produce a response, other treatments to consider include hemodialysis, blood transfusion, exchange transfusion, and hyperbaric oxygen therapy.²

A 66-year-old man presented to the hospital with 3 days of nausea, vomiting, and abdominal pain. He had come to the emergency department several times during this period, but the cause of his symptoms had not been determined.

He had no significant medical history and no previous hospital admissions. He had never undergone colonoscopy and had never taken anticoagulant agents, steroids, laxatives, or nonsteroidal anti-inflammatory drugs.

His abdomen was mildly tender without guarding or rigidity. The standing chest radiograph showed gas under the right diaphragm (Figure 1), and computed tomography (CT) revealed the Chilaiditi sign, with volvulus of the cecum between the diaphragm and liver and a closed-loop obstruction (Figure 2).

The patient was successfully treated with urgent right hemicolectomy.

THE CHILAIDITI SIGN AND SYNDROME

The Chilaiditi sign is an infrequent anomaly found incidentally on chest or abdominal radiography as a colonic interposition between the liver and right hemidiaphragm.¹ It is often asymptomatic but is sometimes accompanied by nausea, vomiting, abdominal pain, and constipation, ie, Chilaiditi syndrome.

Generally, after conservative treatment with fasting and pain control, symptoms may subside and follow-up should be sufficient. However, nasogastric decompression and laxatives are occasionally needed and are often effective in patients with Chilaiditi syndrome. Urgent abdominal surgery is indicated for patients with symptoms of volvulus of the colon, stomach, or small intestine.²

DISTINGUISHING CHARACTERISTICS

The Chilaiditi sign is often confused with pneumoperitoneum, which usually requires urgent abdominal surgery. But the presence of haustration or valvulae conniventes (folds in the small bowel mucosa) in the hepatodiaphragmatic space helps distinguish between intraluminal gas and free air. If the patient presents with abdominal pain without signs of peritonitis, and if imaging indicates the Chilaiditi sign, then supplementary imaging (eg, decubitus radiography, chest CT, abdominal CT) is recommended to make the definitive diagnosis and to avoid unnecessary surgery.

Gas under the diaphragm on standing chest radiography without signs of peritonitis may also be seen after laparotomy and after scuba diving as well as in cases of biliary enteric fistula, incompetent sphincter of Oddi, gallstone ileus, and pneumatosis cystoides intestinalis. The incidence rate of the Chilaiditi sign detected by radiography is between 0.025% and 0.28%.³

PREDISPOSING FACTORS

The cause of the Chilaiditi sign remains unknown. Predisposing factors can be categorized as diaphragmatic (diaphragmatic thinning, phrenic nerve injury, expanded thoracic cavity), intestinal (megacolon, increased intra-abdominal pressure), and hepatic (hepatic atrophy, cirrhosis, ascites).

In healthy people, Chilaiditi syndrome is usually attributed to a congenital abnormal lengthening of the colon or to undue looseness of ligaments of the colon and liver.

Recognizing the Chilaiditi sign is particularly important in patients scheduled to undergo a percutaneous transhepatic procedure or colonoscopic examination, as these procedures increase the risk of perforation.

A 66-year-old man presented to the hospital with 3 days of nausea, vomiting, and abdominal pain. He had come to the emergency department several times during this period, but the cause of his symptoms had not been determined.

He had no significant medical history and no previous hospital admissions. He had never undergone colonoscopy and had never taken anticoagulant agents, steroids, laxatives, or nonsteroidal anti-inflammatory drugs.

His abdomen was mildly tender without guarding or rigidity. The standing chest radiograph showed gas under the right diaphragm (Figure 1), and computed tomography (CT) revealed the Chilaiditi sign, with volvulus of the cecum between the diaphragm and liver and a closed-loop obstruction (Figure 2).

The patient was successfully treated with urgent right hemicolectomy.

THE CHILAIDITI SIGN AND SYNDROME

The Chilaiditi sign is an infrequent anomaly found incidentally on chest or abdominal radiography as a colonic interposition between the liver and right hemidiaphragm.¹ It is often asymptomatic but is sometimes accompanied by nausea, vomiting, abdominal pain, and constipation, ie, Chilaiditi syndrome.

Generally, after conservative treatment with fasting and pain control, symptoms may subside and follow-up should be sufficient. However, nasogastric decompression and laxatives are occasionally needed and are often effective in patients with Chilaiditi syndrome. Urgent abdominal surgery is indicated for patients with symptoms of volvulus of the colon, stomach, or small intestine.²

DISTINGUISHING CHARACTERISTICS

The Chilaiditi sign is often confused with pneumoperitoneum, which usually requires urgent abdominal surgery. But the presence of haustration or valvulae conniventes (folds in the small bowel mucosa) in the hepatodiaphragmatic space helps distinguish between intraluminal gas and free air. If the patient presents with abdominal pain without signs of peritonitis, and if imaging indicates the Chilaiditi sign, then supplementary imaging (eg, decubitus radiography, chest CT, abdominal CT) is recommended to make the definitive diagnosis and to avoid unnecessary surgery.

Gas under the diaphragm on standing chest radiography without signs of peritonitis may also be seen after laparotomy and after scuba diving as well as in cases of biliary enteric fistula, incompetent sphincter of Oddi, gallstone ileus, and pneumatosis cystoides intestinalis. The incidence rate of the Chilaiditi sign detected by radiography is between 0.025% and 0.28%.³

PREDISPOSING FACTORS

The cause of the Chilaiditi sign remains unknown. Predisposing factors can be categorized as diaphragmatic (diaphragmatic thinning, phrenic nerve injury, expanded thoracic cavity), intestinal (megacolon, increased intra-abdominal pressure), and hepatic (hepatic atrophy, cirrhosis, ascites).

In healthy people, Chilaiditi syndrome is usually attributed to a congenital abnormal lengthening of the colon or to undue looseness of ligaments of the colon and liver.

Recognizing the Chilaiditi sign is particularly important in patients scheduled to undergo a percutaneous transhepatic procedure or colonoscopic examination, as these procedures increase the risk of perforation.

A 66-year-old man presented to the hospital with 3 days of nausea, vomiting, and abdominal pain. He had come to the emergency department several times during this period, but the cause of his symptoms had not been determined.

He had no significant medical history and no previous hospital admissions. He had never undergone colonoscopy and had never taken anticoagulant agents, steroids, laxatives, or nonsteroidal anti-inflammatory drugs.

His abdomen was mildly tender without guarding or rigidity. The standing chest radiograph showed gas under the right diaphragm (Figure 1), and computed tomography (CT) revealed the Chilaiditi sign, with volvulus of the cecum between the diaphragm and liver and a closed-loop obstruction (Figure 2).

The patient was successfully treated with urgent right hemicolectomy.

THE CHILAIDITI SIGN AND SYNDROME

The Chilaiditi sign is an infrequent anomaly found incidentally on chest or abdominal radiography as a colonic interposition between the liver and right hemidiaphragm.¹ It is often asymptomatic but is sometimes accompanied by nausea, vomiting, abdominal pain, and constipation, ie, Chilaiditi syndrome.

Generally, after conservative treatment with fasting and pain control, symptoms may subside and follow-up should be sufficient. However, nasogastric decompression and laxatives are occasionally needed and are often effective in patients with Chilaiditi syndrome. Urgent abdominal surgery is indicated for patients with symptoms of volvulus of the colon, stomach, or small intestine.²

DISTINGUISHING CHARACTERISTICS

The Chilaiditi sign is often confused with pneumoperitoneum, which usually requires urgent abdominal surgery. But the presence of haustration or valvulae conniventes (folds in the small bowel mucosa) in the hepatodiaphragmatic space helps distinguish between intraluminal gas and free air. If the patient presents with abdominal pain without signs of peritonitis, and if imaging indicates the Chilaiditi sign, then supplementary imaging (eg, decubitus radiography, chest CT, abdominal CT) is recommended to make the definitive diagnosis and to avoid unnecessary surgery.

Gas under the diaphragm on standing chest radiography without signs of peritonitis may also be seen after laparotomy and after scuba diving as well as in cases of biliary enteric fistula, incompetent sphincter of Oddi, gallstone ileus, and pneumatosis cystoides intestinalis. The incidence rate of the Chilaiditi sign detected by radiography is between 0.025% and 0.28%.³

PREDISPOSING FACTORS

The cause of the Chilaiditi sign remains unknown. Predisposing factors can be categorized as diaphragmatic (diaphragmatic thinning, phrenic nerve injury, expanded thoracic cavity), intestinal (megacolon, increased intra-abdominal pressure), and hepatic (hepatic atrophy, cirrhosis, ascites).

In healthy people, Chilaiditi syndrome is usually attributed to a congenital abnormal lengthening of the colon or to undue looseness of ligaments of the colon and liver.

Recognizing the Chilaiditi sign is particularly important in patients scheduled to undergo a percutaneous transhepatic procedure or colonoscopic examination, as these procedures increase the risk of perforation.

A 66-year-old woman presented to the   emergency room with pain and bluish discoloration of her left great toe for the past 2 days. She had no history of trauma to the toe or of peripheral vascular disease. She also complained of intermittent abdominal pain for the last 5 months and unintentional weight loss of 8 pounds.

On examination, the left hallux was bluish-purple (Figure 1) with an acral distribution (ie, more affected distally). The other extremities were not affected. There was no difference in temperature between her feet, and distal sensation and peripheral pulses were intact.

Vascular disease was suspected, and the patient was started on systemic anticoagulation. However, chest computed tomography (CT) and conventional angiography showed no aortic disease; vessels were of normal caliber, and no distal filling defects were noted.

A routine evaluation with complete blood cell count, peripheral smear, renal function testing, and urinalysis with eosinophil smear was also unrevealing. An extensive investigation followed, including serum complement testing, assays for antinuclear, antineutrophil cytoplasmic, and anti-Sjögren syndrome A and B antibodies, cryoglobulin testing, and hepatitis B and C virus serology, as well as screening for syphilis and lupus anticoagulant, anticardiolipin, and beta-2 glycoprotein antibodies. The results for all these tests were also unremarkable.

Results of coagulation testing and venous duplex ultrasonography of the legs were normal, and electrocardiography and echocardiography showed no signs of valvular vegetation, myxoma, or patent foramen ovale.

Given our patient’s age, abdominal pain, and weight loss but negative vascular evaluation, we considered a diagnosis of paraneoplastic acral vascular syndrome. Abdominal CT revealed a tumor of the pancreatic head with multiple liver lesions, and cytologic study confirmed pancreatic adenocarcinoma.

DISTANT MARKERS OF MALIGNANCY

Causes of blue toe syndrome to consider in the differential diagnosis include arterial thromboembolism, vasoconstrictive drug use or disorders, vasculitis, and venous thrombosis.¹ These are common and deserve prompt investigation. However, if they are ruled out, a peripheral acral vascular syndrome should be considered. These syndromes present as Raynaud phenomenon, gangrene, or acrocyanosis of the fingers or toes with underlying neoplasia. Unusual features such as sudden onset in a patient over age 50, an acral distribution, and associated symptoms such as unrelated pain and weight loss should spark concern for underlying malignancy.

Paraneoplastic syndromes are defined as signs and symptoms that present distant from the site of malignancy. Dermatoses as markers of internal malignancy are well-established but perplexing clinical entities whose exact causes remain unknown.²

Paraneoplastic acral vascular syndrome is associated with certain cancers, predominantly adenocarcinoma and metastatic disease.³ As in our patient, it usually precedes or is present at the time of diagnosis of internal malignancy. Paraneoplastic dermatosis as the presenting sign of pancreatic cancer is uncommon, and a search of the literature found 1 case report of acral vascular syndrome.⁴ Paraneoplastic dermatoses also include necrolytic migratory erythema, Leser-Trélat syndrome, and acrokeratosis paraneoplastica (Table 1).

Paraneoplastic dermatoses are well recognized as harbingers of metastatic disease.^5,6 Our patient’s story demonstrates need for a thorough diagnostic investigation.

A 66-year-old woman presented to the   emergency room with pain and bluish discoloration of her left great toe for the past 2 days. She had no history of trauma to the toe or of peripheral vascular disease. She also complained of intermittent abdominal pain for the last 5 months and unintentional weight loss of 8 pounds.

On examination, the left hallux was bluish-purple (Figure 1) with an acral distribution (ie, more affected distally). The other extremities were not affected. There was no difference in temperature between her feet, and distal sensation and peripheral pulses were intact.

Vascular disease was suspected, and the patient was started on systemic anticoagulation. However, chest computed tomography (CT) and conventional angiography showed no aortic disease; vessels were of normal caliber, and no distal filling defects were noted.

A routine evaluation with complete blood cell count, peripheral smear, renal function testing, and urinalysis with eosinophil smear was also unrevealing. An extensive investigation followed, including serum complement testing, assays for antinuclear, antineutrophil cytoplasmic, and anti-Sjögren syndrome A and B antibodies, cryoglobulin testing, and hepatitis B and C virus serology, as well as screening for syphilis and lupus anticoagulant, anticardiolipin, and beta-2 glycoprotein antibodies. The results for all these tests were also unremarkable.

Results of coagulation testing and venous duplex ultrasonography of the legs were normal, and electrocardiography and echocardiography showed no signs of valvular vegetation, myxoma, or patent foramen ovale.

Given our patient’s age, abdominal pain, and weight loss but negative vascular evaluation, we considered a diagnosis of paraneoplastic acral vascular syndrome. Abdominal CT revealed a tumor of the pancreatic head with multiple liver lesions, and cytologic study confirmed pancreatic adenocarcinoma.

DISTANT MARKERS OF MALIGNANCY

Causes of blue toe syndrome to consider in the differential diagnosis include arterial thromboembolism, vasoconstrictive drug use or disorders, vasculitis, and venous thrombosis.¹ These are common and deserve prompt investigation. However, if they are ruled out, a peripheral acral vascular syndrome should be considered. These syndromes present as Raynaud phenomenon, gangrene, or acrocyanosis of the fingers or toes with underlying neoplasia. Unusual features such as sudden onset in a patient over age 50, an acral distribution, and associated symptoms such as unrelated pain and weight loss should spark concern for underlying malignancy.

Paraneoplastic syndromes are defined as signs and symptoms that present distant from the site of malignancy. Dermatoses as markers of internal malignancy are well-established but perplexing clinical entities whose exact causes remain unknown.²

Paraneoplastic acral vascular syndrome is associated with certain cancers, predominantly adenocarcinoma and metastatic disease.³ As in our patient, it usually precedes or is present at the time of diagnosis of internal malignancy. Paraneoplastic dermatosis as the presenting sign of pancreatic cancer is uncommon, and a search of the literature found 1 case report of acral vascular syndrome.⁴ Paraneoplastic dermatoses also include necrolytic migratory erythema, Leser-Trélat syndrome, and acrokeratosis paraneoplastica (Table 1).

Paraneoplastic dermatoses are well recognized as harbingers of metastatic disease.^5,6 Our patient’s story demonstrates need for a thorough diagnostic investigation.

A 66-year-old woman presented to the   emergency room with pain and bluish discoloration of her left great toe for the past 2 days. She had no history of trauma to the toe or of peripheral vascular disease. She also complained of intermittent abdominal pain for the last 5 months and unintentional weight loss of 8 pounds.

On examination, the left hallux was bluish-purple (Figure 1) with an acral distribution (ie, more affected distally). The other extremities were not affected. There was no difference in temperature between her feet, and distal sensation and peripheral pulses were intact.

Vascular disease was suspected, and the patient was started on systemic anticoagulation. However, chest computed tomography (CT) and conventional angiography showed no aortic disease; vessels were of normal caliber, and no distal filling defects were noted.

A routine evaluation with complete blood cell count, peripheral smear, renal function testing, and urinalysis with eosinophil smear was also unrevealing. An extensive investigation followed, including serum complement testing, assays for antinuclear, antineutrophil cytoplasmic, and anti-Sjögren syndrome A and B antibodies, cryoglobulin testing, and hepatitis B and C virus serology, as well as screening for syphilis and lupus anticoagulant, anticardiolipin, and beta-2 glycoprotein antibodies. The results for all these tests were also unremarkable.

Results of coagulation testing and venous duplex ultrasonography of the legs were normal, and electrocardiography and echocardiography showed no signs of valvular vegetation, myxoma, or patent foramen ovale.

Given our patient’s age, abdominal pain, and weight loss but negative vascular evaluation, we considered a diagnosis of paraneoplastic acral vascular syndrome. Abdominal CT revealed a tumor of the pancreatic head with multiple liver lesions, and cytologic study confirmed pancreatic adenocarcinoma.

DISTANT MARKERS OF MALIGNANCY

Causes of blue toe syndrome to consider in the differential diagnosis include arterial thromboembolism, vasoconstrictive drug use or disorders, vasculitis, and venous thrombosis.¹ These are common and deserve prompt investigation. However, if they are ruled out, a peripheral acral vascular syndrome should be considered. These syndromes present as Raynaud phenomenon, gangrene, or acrocyanosis of the fingers or toes with underlying neoplasia. Unusual features such as sudden onset in a patient over age 50, an acral distribution, and associated symptoms such as unrelated pain and weight loss should spark concern for underlying malignancy.

Paraneoplastic syndromes are defined as signs and symptoms that present distant from the site of malignancy. Dermatoses as markers of internal malignancy are well-established but perplexing clinical entities whose exact causes remain unknown.²

Paraneoplastic acral vascular syndrome is associated with certain cancers, predominantly adenocarcinoma and metastatic disease.³ As in our patient, it usually precedes or is present at the time of diagnosis of internal malignancy. Paraneoplastic dermatosis as the presenting sign of pancreatic cancer is uncommon, and a search of the literature found 1 case report of acral vascular syndrome.⁴ Paraneoplastic dermatoses also include necrolytic migratory erythema, Leser-Trélat syndrome, and acrokeratosis paraneoplastica (Table 1).

Paraneoplastic dermatoses are well recognized as harbingers of metastatic disease.^5,6 Our patient’s story demonstrates need for a thorough diagnostic investigation.

A 42-year-old man presented to his primary  care physician with chief complaints of fatigue and worsening of severe chronic thoracic and lumbar back pain that he attributed to routine daily activity at his job, not to any specific antecedent trauma. Over-the-counter nonsteroidal anti-inflammatory agents and analgesics had provided moderate pain relief. A heating pad, which he had been using daily, often for several hours at a time, offered significant pain relief.

Physical examination revealed a large, hyperpigmented, dark brown, reticular patch with fine telangiectasias spread diffusely over his thoracic and lumbar back (Figure 1). The patch was nontender and nonblanching. There was no pruritus. The patient confirmed the area of hyperpigmentation corresponded to the area of heating pad use. Given this history and the physical findings, a diagnosis of erythema ab igne was made.

AN UNCOMMON CAUSE OF HYPERPIGMENTATION

Erythema ab igne is an uncommon thermally induced eruption associated with periods of repeated exposure of the skin to warm stimuli. It has been reported after holding a kerosene stove between the knees¹ and after balancing a laptop computer on the thighs,² but hot water bottles and heating pads³ are the most commonly reported causes.

Clinical findings and a compatible history are critical to the diagnosis. The involved area should have a history of heat exposure, followed by the development of asymptomatic persistent erythema and, in long-standing cases, hyperpigmentation in a distinct reticulate (netlike) distribution. Telangiectasias and atrophy may occur in advanced disease. In extreme presentations, bullae may develop.⁴

OTHER POTENTIAL CAUSES

Based on the history and findings on physical examination, conditions to consider in the differential diagnosis can include reticular eruptions such as livedo reticularis (associated with cold temperature changes), hypercoagulable states (antiphospholipid antibody syndrome, Sneddon syndrome), and connective tissue diseases (systemic lupus erythematosus).

Other causes of hyperpigmentation such as postinflammatory hyperpigmentation (associated with a prior eruption) and stasis dermatitis (found in areas of poor venous drainage) may also be considered.

The frequent application of an external agent such as a drug or lotion, or even the use of a heating pad if it is made from rubber or is finished with an allergenic dye, raises the possibility of allergic contact dermatitis, but this was not likely in our patient because of the lack of pruritus and active dermatitis. Repeated application of a stimulus such as a heating pad with frequent rubbing can also precipitate lichen simplex chronicus, with thickened, hyperkeratotic skin. Another cause of hyperpigmentation on the back is notalgia paresthetica, which is typically unilateral, over the shoulder blades, and is associated with pain, pruritus, or other neurologic symptoms. Again, these were not present in our patient.

TREATMENT OPTIONS

The first-line treatment for erythema ab igne is to stop exposure to the offending heat source. The hyperpigmentation may slowly fade over several years. Cosmetic treatments such as laser therapy and depigmenting creams can be tried for persistent hyperpigmentation. Patients may be monitored for the small increased risk of cutaneous malignancies—particularly squamous cell carcinoma—arising within regions of erythema ab igne, particularly if atrophic or nonhealing in nature.

Clinicians should recognize the differential diagnosis of erythema ab igne in the appropriate clinical setting and provide the patient counseling regarding this preventable dermatosis.

A 42-year-old man presented to his primary  care physician with chief complaints of fatigue and worsening of severe chronic thoracic and lumbar back pain that he attributed to routine daily activity at his job, not to any specific antecedent trauma. Over-the-counter nonsteroidal anti-inflammatory agents and analgesics had provided moderate pain relief. A heating pad, which he had been using daily, often for several hours at a time, offered significant pain relief.

Physical examination revealed a large, hyperpigmented, dark brown, reticular patch with fine telangiectasias spread diffusely over his thoracic and lumbar back (Figure 1). The patch was nontender and nonblanching. There was no pruritus. The patient confirmed the area of hyperpigmentation corresponded to the area of heating pad use. Given this history and the physical findings, a diagnosis of erythema ab igne was made.

AN UNCOMMON CAUSE OF HYPERPIGMENTATION

Erythema ab igne is an uncommon thermally induced eruption associated with periods of repeated exposure of the skin to warm stimuli. It has been reported after holding a kerosene stove between the knees¹ and after balancing a laptop computer on the thighs,² but hot water bottles and heating pads³ are the most commonly reported causes.

Clinical findings and a compatible history are critical to the diagnosis. The involved area should have a history of heat exposure, followed by the development of asymptomatic persistent erythema and, in long-standing cases, hyperpigmentation in a distinct reticulate (netlike) distribution. Telangiectasias and atrophy may occur in advanced disease. In extreme presentations, bullae may develop.⁴

OTHER POTENTIAL CAUSES

Based on the history and findings on physical examination, conditions to consider in the differential diagnosis can include reticular eruptions such as livedo reticularis (associated with cold temperature changes), hypercoagulable states (antiphospholipid antibody syndrome, Sneddon syndrome), and connective tissue diseases (systemic lupus erythematosus).

Other causes of hyperpigmentation such as postinflammatory hyperpigmentation (associated with a prior eruption) and stasis dermatitis (found in areas of poor venous drainage) may also be considered.

The frequent application of an external agent such as a drug or lotion, or even the use of a heating pad if it is made from rubber or is finished with an allergenic dye, raises the possibility of allergic contact dermatitis, but this was not likely in our patient because of the lack of pruritus and active dermatitis. Repeated application of a stimulus such as a heating pad with frequent rubbing can also precipitate lichen simplex chronicus, with thickened, hyperkeratotic skin. Another cause of hyperpigmentation on the back is notalgia paresthetica, which is typically unilateral, over the shoulder blades, and is associated with pain, pruritus, or other neurologic symptoms. Again, these were not present in our patient.

TREATMENT OPTIONS

The first-line treatment for erythema ab igne is to stop exposure to the offending heat source. The hyperpigmentation may slowly fade over several years. Cosmetic treatments such as laser therapy and depigmenting creams can be tried for persistent hyperpigmentation. Patients may be monitored for the small increased risk of cutaneous malignancies—particularly squamous cell carcinoma—arising within regions of erythema ab igne, particularly if atrophic or nonhealing in nature.

Clinicians should recognize the differential diagnosis of erythema ab igne in the appropriate clinical setting and provide the patient counseling regarding this preventable dermatosis.

A 42-year-old man presented to his primary  care physician with chief complaints of fatigue and worsening of severe chronic thoracic and lumbar back pain that he attributed to routine daily activity at his job, not to any specific antecedent trauma. Over-the-counter nonsteroidal anti-inflammatory agents and analgesics had provided moderate pain relief. A heating pad, which he had been using daily, often for several hours at a time, offered significant pain relief.

Physical examination revealed a large, hyperpigmented, dark brown, reticular patch with fine telangiectasias spread diffusely over his thoracic and lumbar back (Figure 1). The patch was nontender and nonblanching. There was no pruritus. The patient confirmed the area of hyperpigmentation corresponded to the area of heating pad use. Given this history and the physical findings, a diagnosis of erythema ab igne was made.

AN UNCOMMON CAUSE OF HYPERPIGMENTATION

Erythema ab igne is an uncommon thermally induced eruption associated with periods of repeated exposure of the skin to warm stimuli. It has been reported after holding a kerosene stove between the knees¹ and after balancing a laptop computer on the thighs,² but hot water bottles and heating pads³ are the most commonly reported causes.

Clinical findings and a compatible history are critical to the diagnosis. The involved area should have a history of heat exposure, followed by the development of asymptomatic persistent erythema and, in long-standing cases, hyperpigmentation in a distinct reticulate (netlike) distribution. Telangiectasias and atrophy may occur in advanced disease. In extreme presentations, bullae may develop.⁴

OTHER POTENTIAL CAUSES

Based on the history and findings on physical examination, conditions to consider in the differential diagnosis can include reticular eruptions such as livedo reticularis (associated with cold temperature changes), hypercoagulable states (antiphospholipid antibody syndrome, Sneddon syndrome), and connective tissue diseases (systemic lupus erythematosus).

Other causes of hyperpigmentation such as postinflammatory hyperpigmentation (associated with a prior eruption) and stasis dermatitis (found in areas of poor venous drainage) may also be considered.

The frequent application of an external agent such as a drug or lotion, or even the use of a heating pad if it is made from rubber or is finished with an allergenic dye, raises the possibility of allergic contact dermatitis, but this was not likely in our patient because of the lack of pruritus and active dermatitis. Repeated application of a stimulus such as a heating pad with frequent rubbing can also precipitate lichen simplex chronicus, with thickened, hyperkeratotic skin. Another cause of hyperpigmentation on the back is notalgia paresthetica, which is typically unilateral, over the shoulder blades, and is associated with pain, pruritus, or other neurologic symptoms. Again, these were not present in our patient.

TREATMENT OPTIONS

The first-line treatment for erythema ab igne is to stop exposure to the offending heat source. The hyperpigmentation may slowly fade over several years. Cosmetic treatments such as laser therapy and depigmenting creams can be tried for persistent hyperpigmentation. Patients may be monitored for the small increased risk of cutaneous malignancies—particularly squamous cell carcinoma—arising within regions of erythema ab igne, particularly if atrophic or nonhealing in nature.

Clinicians should recognize the differential diagnosis of erythema ab igne in the appropriate clinical setting and provide the patient counseling regarding this preventable dermatosis.

A 96-year-old woman with hypertension, diabetes,    and dementia was found unresponsive in her nursing home and was transferred to the hospital.

At presentation to the hospital, her blood pressure was 76/43 mm Hg, heart rate 42 beats per minute, rectal temperature 31.6°C (88.8°F), and blood glucose 36 mg/dL.

The initial electrocardiogram (ECG) (Figure 1) showed sinus bradycardia with first-degree atrioventricular block and a PR interval of 704 ms. The QRS interval was mildly increased, and the corrected QT interval was mildly prolonged at 476 ms. There was also evidence of probable small Osborn waves in leads II and V₅, and leads aVF and aVL seemed reversed, as was confirmed in successive ECGs.

The patient was resuscitated with intravenous fluids and glucose and was rewarmed. Repeat ECG 3 hours later (Figure 2) revealed sinus bradycardia with first-degree atrioventricular block and a PR interval of 216 ms with a rate of 52. This time the leads were confirmed in correct position, with aVF showing negative QRS deflection. Q waves were also noted in leads III and aVF, as in previous ECGs, and suggested an old inferior wall infarction. This was not seen on the first ECG because of probable lead reversal, and the suspected Osborn waves were also less prominent in V₅ and absent in lead II. The corrected QT interval was now 465 ms, and her body temperature at this time was 32.8°C (91.0°F).

Causes of secondary hypothermia were sought. Blood and urine cultures were negative. Computed tomography of the head showed no acute intracranial abnormalities. Tests for adrenal insufficiency and hypothyroidism were negative.

HYPOTHERMIA AND THE ECG

Hypothermia can produce a number of changes on the ECG. At the start of hypothermia, a stress reaction is induced, resulting in sinus tachycardia. But when the temperature goes below 32°C, sinus bradycardia ensues,¹ resulting in various degrees of heart block.² In our patient, a severely prolonged PR interval resulted in first-degree heart block.

Other findings on ECG associated with hypothermia include atrial fibrillation, widening of the P and T waves, prolonging of the QT interval, and widening of the QRS interval. Progressive widening of the QRS interval can predispose to ventricular fibrillation.^1,3

An Osborn or J wave is a wave found between the end of the QRS and the beginning of the ST segment and is usually seen on the inferior and lateral precordial leads. It is found in as many as 80% of patients when the body temperature is below 30°C.^1,3,4

Although Osborn waves are a common finding in hypothermia, they are also seen in electrolyte imbalances such as hypercalcemia and in central nervous system diseases.^5,6 Hypothermia-associated changes on ECG are usually readily reversible with rewarming.¹

TAKE-HOME MESSAGES

The ECG should always be interpreted in the proper clinical context and, whenever possible, compared with a previous ECG. It is prudent to always consider potentially reversible triggers of hypothermia other than environmental exposure such as hypothyroidism, infection, adrenal insufficiency, ketoacidosis, medication side effects, and alcohol use.

Hypothermia, especially in elderly patients with multiple comorbidities, can lead to bradycardia and varying degrees of heart block.

A 96-year-old woman with hypertension, diabetes,    and dementia was found unresponsive in her nursing home and was transferred to the hospital.

At presentation to the hospital, her blood pressure was 76/43 mm Hg, heart rate 42 beats per minute, rectal temperature 31.6°C (88.8°F), and blood glucose 36 mg/dL.

The initial electrocardiogram (ECG) (Figure 1) showed sinus bradycardia with first-degree atrioventricular block and a PR interval of 704 ms. The QRS interval was mildly increased, and the corrected QT interval was mildly prolonged at 476 ms. There was also evidence of probable small Osborn waves in leads II and V₅, and leads aVF and aVL seemed reversed, as was confirmed in successive ECGs.

The patient was resuscitated with intravenous fluids and glucose and was rewarmed. Repeat ECG 3 hours later (Figure 2) revealed sinus bradycardia with first-degree atrioventricular block and a PR interval of 216 ms with a rate of 52. This time the leads were confirmed in correct position, with aVF showing negative QRS deflection. Q waves were also noted in leads III and aVF, as in previous ECGs, and suggested an old inferior wall infarction. This was not seen on the first ECG because of probable lead reversal, and the suspected Osborn waves were also less prominent in V₅ and absent in lead II. The corrected QT interval was now 465 ms, and her body temperature at this time was 32.8°C (91.0°F).

Causes of secondary hypothermia were sought. Blood and urine cultures were negative. Computed tomography of the head showed no acute intracranial abnormalities. Tests for adrenal insufficiency and hypothyroidism were negative.

HYPOTHERMIA AND THE ECG

Hypothermia can produce a number of changes on the ECG. At the start of hypothermia, a stress reaction is induced, resulting in sinus tachycardia. But when the temperature goes below 32°C, sinus bradycardia ensues,¹ resulting in various degrees of heart block.² In our patient, a severely prolonged PR interval resulted in first-degree heart block.

Other findings on ECG associated with hypothermia include atrial fibrillation, widening of the P and T waves, prolonging of the QT interval, and widening of the QRS interval. Progressive widening of the QRS interval can predispose to ventricular fibrillation.^1,3

An Osborn or J wave is a wave found between the end of the QRS and the beginning of the ST segment and is usually seen on the inferior and lateral precordial leads. It is found in as many as 80% of patients when the body temperature is below 30°C.^1,3,4

Although Osborn waves are a common finding in hypothermia, they are also seen in electrolyte imbalances such as hypercalcemia and in central nervous system diseases.^5,6 Hypothermia-associated changes on ECG are usually readily reversible with rewarming.¹

TAKE-HOME MESSAGES

The ECG should always be interpreted in the proper clinical context and, whenever possible, compared with a previous ECG. It is prudent to always consider potentially reversible triggers of hypothermia other than environmental exposure such as hypothyroidism, infection, adrenal insufficiency, ketoacidosis, medication side effects, and alcohol use.

Hypothermia, especially in elderly patients with multiple comorbidities, can lead to bradycardia and varying degrees of heart block.

A 96-year-old woman with hypertension, diabetes,    and dementia was found unresponsive in her nursing home and was transferred to the hospital.

At presentation to the hospital, her blood pressure was 76/43 mm Hg, heart rate 42 beats per minute, rectal temperature 31.6°C (88.8°F), and blood glucose 36 mg/dL.

The initial electrocardiogram (ECG) (Figure 1) showed sinus bradycardia with first-degree atrioventricular block and a PR interval of 704 ms. The QRS interval was mildly increased, and the corrected QT interval was mildly prolonged at 476 ms. There was also evidence of probable small Osborn waves in leads II and V₅, and leads aVF and aVL seemed reversed, as was confirmed in successive ECGs.

The patient was resuscitated with intravenous fluids and glucose and was rewarmed. Repeat ECG 3 hours later (Figure 2) revealed sinus bradycardia with first-degree atrioventricular block and a PR interval of 216 ms with a rate of 52. This time the leads were confirmed in correct position, with aVF showing negative QRS deflection. Q waves were also noted in leads III and aVF, as in previous ECGs, and suggested an old inferior wall infarction. This was not seen on the first ECG because of probable lead reversal, and the suspected Osborn waves were also less prominent in V₅ and absent in lead II. The corrected QT interval was now 465 ms, and her body temperature at this time was 32.8°C (91.0°F).

Causes of secondary hypothermia were sought. Blood and urine cultures were negative. Computed tomography of the head showed no acute intracranial abnormalities. Tests for adrenal insufficiency and hypothyroidism were negative.

HYPOTHERMIA AND THE ECG

Hypothermia can produce a number of changes on the ECG. At the start of hypothermia, a stress reaction is induced, resulting in sinus tachycardia. But when the temperature goes below 32°C, sinus bradycardia ensues,¹ resulting in various degrees of heart block.² In our patient, a severely prolonged PR interval resulted in first-degree heart block.

Other findings on ECG associated with hypothermia include atrial fibrillation, widening of the P and T waves, prolonging of the QT interval, and widening of the QRS interval. Progressive widening of the QRS interval can predispose to ventricular fibrillation.^1,3

An Osborn or J wave is a wave found between the end of the QRS and the beginning of the ST segment and is usually seen on the inferior and lateral precordial leads. It is found in as many as 80% of patients when the body temperature is below 30°C.^1,3,4

Although Osborn waves are a common finding in hypothermia, they are also seen in electrolyte imbalances such as hypercalcemia and in central nervous system diseases.^5,6 Hypothermia-associated changes on ECG are usually readily reversible with rewarming.¹

TAKE-HOME MESSAGES

The ECG should always be interpreted in the proper clinical context and, whenever possible, compared with a previous ECG. It is prudent to always consider potentially reversible triggers of hypothermia other than environmental exposure such as hypothyroidism, infection, adrenal insufficiency, ketoacidosis, medication side effects, and alcohol use.

Hypothermia, especially in elderly patients with multiple comorbidities, can lead to bradycardia and varying degrees of heart block.