Critical illness Polyneuropathy

The most common causes of acute generalized weakness leading to admission to a medical intensive care unit (ICU) are GBS and myasthenia gravis However, weakness developing in critically ill patients while in the ICU is usually caused by critical illness polyneuropathy (CIP) or critical illness myopathy (CIM), or much less commonly, by prolonged neuromuscular blockade. Both CIM and CIP develop as a complication of sepsis and multiple organ failure. They usually present as an inability to wean a patient from a ventilator. A coexisting encephalopathy may limit the neurologic exam, in particular the sensory examination. Muscle stretch reflexes are absent or reduced.
CIP was first described by Charles F. Bolton in a series of five patients.
Critical illness Polyneuropathy


The causes of CIP and CIM are unknown, though they are thought to be a possible neurological manifestation of systemic inflammatory response syndrome.[2]
Unlike Guillain Barre Syndrome, another neurological disorder that causes weakness, patients with critical illness polyneuropathy do not have loss of the myelin sheath that normally surrounds neurons (demyelination).

Signs and symptoms

People with CIP/CIM have progressive, generalized, symmetric muscle weakness. CIP/CIM typically develops in the setting of a critical illness and immobilization, so patients with CIP/CIM are often receiving treatment in the intensive care unit (ICU).
Weakness (motor deficits) occurs in generalized fashion, rather than beginning in one region of the body and spreading. The hip and shoulder muscles are especially affected. The muscles of the face are usually spared, but in rare cases, the eye muscles may be weakened, leading to ophthalmoplegia.
Respiratory difficulties can be caused by atrophy of the muscles between the ribs (intercostals), atrophy of the diaphragm muscle, and degeneration of the nerve that stimulates the diaphragm (phrenic nerve).This can prolong the time the wean a person off of a breathing machine (mechanical ventilation) by as much as 7 – 13 days.

Laboratory values

The serum creatine phosphokinase (CPK) is usually mildly elevated.[7] While the CPK is often a good marker for damage to muscle tissue, it is not a helpful marker in CIP/CIM, because CIP/CIM is a gradual process and does not usually involve significant muscle cell death (necrosis). Also, even if necrosis is present, it may be brief and is therefore easily missed. If a lumbar puncture (spinal tap) is performed, the protein level in the cerebral spinal fluid would be normal.


The diagnosis of CIP/CIM is a clinical diagnosis, as there is no single laboratory or imaging test available to detect CIP/CIM.
CIP/CIM is often not identified until a patient is unable to be successfully weaned from a mechanical ventilator. Early detection of the condition is difficult, because these patients are often sedated and intubated, and thus unable to cooperate with a thorough neuromuscular physical examination.Furthermore, the use of nerve conduction studies is difficult when there is overlying tissue edema, which is often present in patients in the intensive care unit.


While the exact incidence is unknown, estimates range from 33 – 57 percent of patients staying in the ICU for longer than 7 days. More exact data is difficult to obtainThe three main risk factors for CIP and CIM are sepsis and systemic inflammatory response syndrome (SIRS), and multi-organ failure. Reported rates of CIP/CIM in in people with sepsis and SIRS range from 68 to 100 percent. Additional risk factors for developing CIP/CIM include: female gender, high blood sugar (hyperglycemia), low serum albumin, and immobility. A greater severity of illness increases the risk of CIP/CIM. Such risk factors include: multi-organ dysfunction, renal failure, renal replacement therapy, duration of organ dysfunction, duration of ICU stay, low albumin, and central neurologic failure.
Certain medications are associated with CIP/CIM, such as corticosteroids, neuromuscular blocking agents, vasopressors, catecholamines, and intravenous nutrition (parenteral nutrition). Research has produced inconsistent results for the impact of hypoxia, hypotension, hyperpyrexia, and increased age on the risk of CIP/CIM. The use of aminoglycosides is not an independent risk for the development of CIP/CIM.


CIP/CIM can lead to difficulty weaning a person from a mechanical ventilator, and is associated with increased length of stay in the ICU and increased mortality (death).] It can lead to impaired rehabilitation. Since CIP/CIM can lead to decreased mobility (movement), it increases the risk of pneumonia, deep vein thrombosis, and pulmonary embolism.Critically ill people that are in a coma can become completely paralyzed from CIP/CIM. Improvement usually occurs in weeks to months, as the innervation to the muscles are restored. About half of patients recover fully.