Case Studies in Toxicology: One Last Kick—Transverse Myelitis After an Overdose of Heroin via Insufflation

Case

A 17-year-old adolescent girl with a history of depression and opioid dependence, for which she was taking buprenorphine until 2 weeks earlier, presented to the ED via emergency medical services (EMS) after her father found her lying on the couch unresponsive and with shallow respirations. Naloxone was administered by EMS and her mental status improved.

At presentation, the patient admitted to insufflation of an unknown amount of heroin and ingestion of 2 mg of alprazolam earlier in the day. She denied any past or current use of intravenous (IV) drugs. During monitoring, she began to complain of numbness in her legs and an inability to urinate. Examination revealed paralysis and decreased sensation of her bilateral lower extremities to the midthigh, with decreased rectal tone. Because of the patient’s history of drug use and temporal association with the heroin overdose, both neurosurgery and toxicology services were consulted.

What can cause lower extremity paralysis in a drug user?

The differential diagnosis for the patient at this point included toxin-induced myelopathy, Guillain-Barré syndrome, hypokalemic periodic paralysis, spinal compression, epidural abscess, cerebrovascular accident, spinal lesion, and spinal artery dissection or infarction.

Although Guillain-Barré syndrome presents with ascending paralysis, there is usually an antecedent respiratory or gastrointestinal infection. While epidural abscess with spinal compression is associated with IV drug use and can present similarly, the patient in this case denied IV use. In the absence of any risk factors, cerebrovascular accident and spinal artery dissection were also unlikely.

Case Continuation

A bladder catheter was placed due to the patient’s inability to urinate, and approximately 1 L of urine output was retrieved. Immediate magnetic resonance imaging (MRI) demonstrated increased T2 signal intensity and expansion of the distal thoracic cord and conus without mass lesion, consistent with transverse myelitis (TM).

What is transverse myelitis and why does it occur?

Transverse myelitis is an inflammatory demyelinating disorder that focally affects the spinal cord, resulting in a specific pattern of motor, sensory, and autonomic dysfunction.¹ Signs and symptoms include paresthesia, paralysis of the extremities, and loss of bladder and bowel control. The level of the spinal cord affected determines the clinical effects. Demyelination typically occurs at the thoracic segment, producing findings in the legs, as well as bladder and bowel dysfunction. 

The exact cause of TM is unknown, but the inflammation may result from a viral complication or an abnormal immune response. Infectious viral agents suspected of causing TM include varicella zoster, herpes simplex, cytomegalovirus, Epstein-Barr, influenza, human immunodeficiency virus, hepatitis A, and rubella. It has also been postulated that an autoimmune reaction is responsible for the condition.

In some individuals, TM represents the first manifestation of an underlying demyelinating disorder such as multiple sclerosis or neuromyelitis optica. A diagnosis of TM is made through patient history, physical examination, and characteristic findings on neuroimaging, specifically MRI.

Heroin use has long been associated with the development of TM, and is usually associated with IV administration of the drug after a period of abstinence.² This association strengthens the basis for an immunologic etiology—an initial sensitization and subsequent reexposure causing the effects of TM. There have also been cases of TM coexisting with rhabdomyolysis due to the patient being found in a contorted position.³ Another theory of the etiology of heroin-associated TM is a reaction to a possible adulterant or contaminant in the heroin.⁴

What is the treatment and prognosis of transverse myelitis?

Since there is no cure for TM, treatment is directed at reducing inflammation in the spinal cord. Initial therapy generally includes corticosteroids. In patients with a minimal response to corticosteroids, plasma exchange can be attempted. There are also limited data to suggest a beneficial role for the use of IV immunoglobulin.⁵ In addition to treatment, general supportive care must also be optimized, such as the use of prophylaxis for thrombophlebitis due to immobility and physical therapy, if possible.

The prognosis of patients with TM is variable, and up to two thirds of patients will have moderate-to-severe residual neurological disability.⁶ Recovery is slow, with most patients beginning to show improvement within the first 2 to 12 weeks from treatment and supportive care. The recovery process can continue for 2 years. However, if no improvement is made within the first 3 to 6 months, recovery is unlikely.⁷ Cases of heroin-associated TM may have a more favorable prognosis.⁸

A majority of individuals will only experience this clinical entity once, but there are rare causes of recurrent or relapsing TM.⁷ In these situations, a search for underlying demyelinating diseases should be performed.

Case Conclusion 

The patient was immediately started on IV corticosteroids, but as there was no improvement after 5 days, plasmapheresis was performed. She received 5 cycles of plasmapheresis and a 5-day course of IV immunoglobulin but still without any improvement. A repeat MRI of the thoracic spine was performed and raised the possibility of cord infarct, but infectious or inflammatory myelitis remained within differential consideration. The patient continued to make minimal improvement with physical therapy and, after a 3-week hospital course, she was transferred to inpatient rehabilitation for further care. Over the next 2 months, the loss of sensation and motor ability of her legs did not improve, but she did regain control of her bowels and bladder.

Dr Regina is a medical toxicology fellow in the department of emergency medicine at North Shore Long Island Jewish Health System, New York. Dr Nelson, editor of “Case Studies in Toxicology,” is a professor in the department of emergency medicine and director of the medical toxicology fellowship program at the New York University School of Medicine and the New York City Poison Control Center. He is also associate editor, toxicology, of the EMERGENCY MEDICINE editorial board.

Case

A 17-year-old adolescent girl with a history of depression and opioid dependence, for which she was taking buprenorphine until 2 weeks earlier, presented to the ED via emergency medical services (EMS) after her father found her lying on the couch unresponsive and with shallow respirations. Naloxone was administered by EMS and her mental status improved.

At presentation, the patient admitted to insufflation of an unknown amount of heroin and ingestion of 2 mg of alprazolam earlier in the day. She denied any past or current use of intravenous (IV) drugs. During monitoring, she began to complain of numbness in her legs and an inability to urinate. Examination revealed paralysis and decreased sensation of her bilateral lower extremities to the midthigh, with decreased rectal tone. Because of the patient’s history of drug use and temporal association with the heroin overdose, both neurosurgery and toxicology services were consulted.

What can cause lower extremity paralysis in a drug user?

The differential diagnosis for the patient at this point included toxin-induced myelopathy, Guillain-Barré syndrome, hypokalemic periodic paralysis, spinal compression, epidural abscess, cerebrovascular accident, spinal lesion, and spinal artery dissection or infarction.

Although Guillain-Barré syndrome presents with ascending paralysis, there is usually an antecedent respiratory or gastrointestinal infection. While epidural abscess with spinal compression is associated with IV drug use and can present similarly, the patient in this case denied IV use. In the absence of any risk factors, cerebrovascular accident and spinal artery dissection were also unlikely.

Case Continuation

A bladder catheter was placed due to the patient’s inability to urinate, and approximately 1 L of urine output was retrieved. Immediate magnetic resonance imaging (MRI) demonstrated increased T2 signal intensity and expansion of the distal thoracic cord and conus without mass lesion, consistent with transverse myelitis (TM).

What is transverse myelitis and why does it occur?

Transverse myelitis is an inflammatory demyelinating disorder that focally affects the spinal cord, resulting in a specific pattern of motor, sensory, and autonomic dysfunction.¹ Signs and symptoms include paresthesia, paralysis of the extremities, and loss of bladder and bowel control. The level of the spinal cord affected determines the clinical effects. Demyelination typically occurs at the thoracic segment, producing findings in the legs, as well as bladder and bowel dysfunction. 

The exact cause of TM is unknown, but the inflammation may result from a viral complication or an abnormal immune response. Infectious viral agents suspected of causing TM include varicella zoster, herpes simplex, cytomegalovirus, Epstein-Barr, influenza, human immunodeficiency virus, hepatitis A, and rubella. It has also been postulated that an autoimmune reaction is responsible for the condition.

In some individuals, TM represents the first manifestation of an underlying demyelinating disorder such as multiple sclerosis or neuromyelitis optica. A diagnosis of TM is made through patient history, physical examination, and characteristic findings on neuroimaging, specifically MRI.

Heroin use has long been associated with the development of TM, and is usually associated with IV administration of the drug after a period of abstinence.² This association strengthens the basis for an immunologic etiology—an initial sensitization and subsequent reexposure causing the effects of TM. There have also been cases of TM coexisting with rhabdomyolysis due to the patient being found in a contorted position.³ Another theory of the etiology of heroin-associated TM is a reaction to a possible adulterant or contaminant in the heroin.⁴

What is the treatment and prognosis of transverse myelitis?

Since there is no cure for TM, treatment is directed at reducing inflammation in the spinal cord. Initial therapy generally includes corticosteroids. In patients with a minimal response to corticosteroids, plasma exchange can be attempted. There are also limited data to suggest a beneficial role for the use of IV immunoglobulin.⁵ In addition to treatment, general supportive care must also be optimized, such as the use of prophylaxis for thrombophlebitis due to immobility and physical therapy, if possible.

The prognosis of patients with TM is variable, and up to two thirds of patients will have moderate-to-severe residual neurological disability.⁶ Recovery is slow, with most patients beginning to show improvement within the first 2 to 12 weeks from treatment and supportive care. The recovery process can continue for 2 years. However, if no improvement is made within the first 3 to 6 months, recovery is unlikely.⁷ Cases of heroin-associated TM may have a more favorable prognosis.⁸

A majority of individuals will only experience this clinical entity once, but there are rare causes of recurrent or relapsing TM.⁷ In these situations, a search for underlying demyelinating diseases should be performed.

Case Conclusion 

The patient was immediately started on IV corticosteroids, but as there was no improvement after 5 days, plasmapheresis was performed. She received 5 cycles of plasmapheresis and a 5-day course of IV immunoglobulin but still without any improvement. A repeat MRI of the thoracic spine was performed and raised the possibility of cord infarct, but infectious or inflammatory myelitis remained within differential consideration. The patient continued to make minimal improvement with physical therapy and, after a 3-week hospital course, she was transferred to inpatient rehabilitation for further care. Over the next 2 months, the loss of sensation and motor ability of her legs did not improve, but she did regain control of her bowels and bladder.

Dr Regina is a medical toxicology fellow in the department of emergency medicine at North Shore Long Island Jewish Health System, New York. Dr Nelson, editor of “Case Studies in Toxicology,” is a professor in the department of emergency medicine and director of the medical toxicology fellowship program at the New York University School of Medicine and the New York City Poison Control Center. He is also associate editor, toxicology, of the EMERGENCY MEDICINE editorial board.

Case

A 17-year-old adolescent girl with a history of depression and opioid dependence, for which she was taking buprenorphine until 2 weeks earlier, presented to the ED via emergency medical services (EMS) after her father found her lying on the couch unresponsive and with shallow respirations. Naloxone was administered by EMS and her mental status improved.

At presentation, the patient admitted to insufflation of an unknown amount of heroin and ingestion of 2 mg of alprazolam earlier in the day. She denied any past or current use of intravenous (IV) drugs. During monitoring, she began to complain of numbness in her legs and an inability to urinate. Examination revealed paralysis and decreased sensation of her bilateral lower extremities to the midthigh, with decreased rectal tone. Because of the patient’s history of drug use and temporal association with the heroin overdose, both neurosurgery and toxicology services were consulted.

What can cause lower extremity paralysis in a drug user?

The differential diagnosis for the patient at this point included toxin-induced myelopathy, Guillain-Barré syndrome, hypokalemic periodic paralysis, spinal compression, epidural abscess, cerebrovascular accident, spinal lesion, and spinal artery dissection or infarction.

Although Guillain-Barré syndrome presents with ascending paralysis, there is usually an antecedent respiratory or gastrointestinal infection. While epidural abscess with spinal compression is associated with IV drug use and can present similarly, the patient in this case denied IV use. In the absence of any risk factors, cerebrovascular accident and spinal artery dissection were also unlikely.

Case Continuation

A bladder catheter was placed due to the patient’s inability to urinate, and approximately 1 L of urine output was retrieved. Immediate magnetic resonance imaging (MRI) demonstrated increased T2 signal intensity and expansion of the distal thoracic cord and conus without mass lesion, consistent with transverse myelitis (TM).

What is transverse myelitis and why does it occur?

Transverse myelitis is an inflammatory demyelinating disorder that focally affects the spinal cord, resulting in a specific pattern of motor, sensory, and autonomic dysfunction.¹ Signs and symptoms include paresthesia, paralysis of the extremities, and loss of bladder and bowel control. The level of the spinal cord affected determines the clinical effects. Demyelination typically occurs at the thoracic segment, producing findings in the legs, as well as bladder and bowel dysfunction. 

The exact cause of TM is unknown, but the inflammation may result from a viral complication or an abnormal immune response. Infectious viral agents suspected of causing TM include varicella zoster, herpes simplex, cytomegalovirus, Epstein-Barr, influenza, human immunodeficiency virus, hepatitis A, and rubella. It has also been postulated that an autoimmune reaction is responsible for the condition.

In some individuals, TM represents the first manifestation of an underlying demyelinating disorder such as multiple sclerosis or neuromyelitis optica. A diagnosis of TM is made through patient history, physical examination, and characteristic findings on neuroimaging, specifically MRI.

Heroin use has long been associated with the development of TM, and is usually associated with IV administration of the drug after a period of abstinence.² This association strengthens the basis for an immunologic etiology—an initial sensitization and subsequent reexposure causing the effects of TM. There have also been cases of TM coexisting with rhabdomyolysis due to the patient being found in a contorted position.³ Another theory of the etiology of heroin-associated TM is a reaction to a possible adulterant or contaminant in the heroin.⁴

What is the treatment and prognosis of transverse myelitis?

Since there is no cure for TM, treatment is directed at reducing inflammation in the spinal cord. Initial therapy generally includes corticosteroids. In patients with a minimal response to corticosteroids, plasma exchange can be attempted. There are also limited data to suggest a beneficial role for the use of IV immunoglobulin.⁵ In addition to treatment, general supportive care must also be optimized, such as the use of prophylaxis for thrombophlebitis due to immobility and physical therapy, if possible.

The prognosis of patients with TM is variable, and up to two thirds of patients will have moderate-to-severe residual neurological disability.⁶ Recovery is slow, with most patients beginning to show improvement within the first 2 to 12 weeks from treatment and supportive care. The recovery process can continue for 2 years. However, if no improvement is made within the first 3 to 6 months, recovery is unlikely.⁷ Cases of heroin-associated TM may have a more favorable prognosis.⁸

A majority of individuals will only experience this clinical entity once, but there are rare causes of recurrent or relapsing TM.⁷ In these situations, a search for underlying demyelinating diseases should be performed.

Case Conclusion 

The patient was immediately started on IV corticosteroids, but as there was no improvement after 5 days, plasmapheresis was performed. She received 5 cycles of plasmapheresis and a 5-day course of IV immunoglobulin but still without any improvement. A repeat MRI of the thoracic spine was performed and raised the possibility of cord infarct, but infectious or inflammatory myelitis remained within differential consideration. The patient continued to make minimal improvement with physical therapy and, after a 3-week hospital course, she was transferred to inpatient rehabilitation for further care. Over the next 2 months, the loss of sensation and motor ability of her legs did not improve, but she did regain control of her bowels and bladder.

Dr Regina is a medical toxicology fellow in the department of emergency medicine at North Shore Long Island Jewish Health System, New York. Dr Nelson, editor of “Case Studies in Toxicology,” is a professor in the department of emergency medicine and director of the medical toxicology fellowship program at the New York University School of Medicine and the New York City Poison Control Center. He is also associate editor, toxicology, of the EMERGENCY MEDICINE editorial board.