From Bad to Worse
Answer: C
This man has suffered a subarachnoid hemorrhage (SAH), which may or may not be associated with an aneurysm. Cocaine use causes abrupt large increases in blood pressure causing a rent in the arterial vasculature.
First a quick review: various scales are used to grade and prognosticate SAH, the most common of which are the Hunt and Hess scale and the World Federation of Neurological Surgeons (WFNS) scale. The Hunt and Hess scale is popular among emergency physicians for its ease of use and that it has been well studied:
Grade Neurologic status
1 Asymptomatic or mild headache and slight nuchal rigidity
2 Severe headache, stiff neck, no neurologic deficit except cranial nerve palsy
3 Drowsy or confused, mild focal neurologic deficit
4 Stuporous, moderate or severe hemiparesis
5 Coma, decerebrate posturing
Hunt and Hess grade 1 is associated with a 70% survival rate. Subsequent studies found similar survival rates between grades 1 and 2 (although this may have to do with problems of classification – the correlation
coefficient, κ, in a pooled analysis was 0.46, only moderate agreement). The key point here is that there is a
50% and higher mortality for grade 3 and above.
The WFNS scale offers the added advantage of incorporating GCS (arguably less subjective – κ in WFNS ranges from 0.27 to 0.6); however, it is more complicated and may be more difficult to remember:
Grade GCS score Motor deficit
1 15 Absent
2 13 to 14 Absent
3 13 to 14 Present
4 7 to 12 Present or absent
5 3 to 6 Present or absent
Some studies demonstrate that WFNS mortality steadily increases from grade 1 to grade 5, while others challenge its prognostic ability.
Our patient is experiencing neurogenic pulmonary edema (NPE), a type of non-cardiogenic pulmonary edema (i.e. a clinical diagnosis made by the presence of radiographic evidence of alveolar fluid accumulation without hemodynamic evidence to suggest a cardiogenic etiology – if measured, pulmonary artery wedge pressure ≤ 18 mmHg).
Neurogenic pulmonary edema may be caused by status epilepticus, head injury, or cerebral hemorrhage.
The pathophysiology of NPE is poorly understood. The theory is that a sympathetic surge from the medulla oblongata causes a neurologically mediated pulmonary venoconstriction, which increases the pulmonary capillary hydrostatic pressure and results in pulmonary edema.
It is important to distinguish non-cardiogenic pulmonary edema (here, the specific case of neurogenic
pulmonary edema) from cardiogenic pulmonary edema. Diuresis (B) would be a good choice for cardiogenic pulmonary edema due to volume overload, but may have untoward hemodynamic consequences in this setting of NPE. Although the presentation of acute respiratory distress syndrome (ARDS) may mimic NPE, ARDS protocols call for low tidal volumes and increasing PEEP (A) (i.e. rather than simply increasing the FiO2). Increasing PEEP in NPE should be used with extreme caution (and really only after an intracranial pressure monitor is placed), as it has been linked to decreased cerebral perfusion pressure and worsening outcomes (due to increased intrathoracic pressure, decreased venous return, systemic hypoperfusion).
Peak pressures may be elevated in lung parenchymal disease, especially if the plateau pressure is also elevated (as an aside, if the plateau pressure is normal and the peak pressure only is elevated, think airway obstruction). Unfortunately here, a slower respiratory rate (D) may inadvertently allow for hypercapnia, which would cause cerebral vasodilation and worsening intracranial pressure (perpetuating the vicious cycle of NPE). Further, slowing the respiratory rate (by increasing the expiratory time) is a strategy to improve auto-PEEP and breath-stacking (not to decrease the peak inspiratory pressure).
In distinction from other type of pulmonary edema, management of neurogenic pulmonary edema requires optimization of the primary neurologic insult and supportive care.
Prone positioning (C) is a tried-and-true adjunct to improve oxygenation in ventilated patients suffering
from a variety of pulmonary problems: dependent areas are better oxygenated. Also called the lung recruitment maneuver, prone positioning in mechanically ventilated patients optimizes functional residual capacity, redistributes blood flow (minimizes V-Q mismatch), aids in diaphragm excursion, and improves secretion removal. It is a natural way to improve oxygenation and ventilation without untoward physiologic consequences (as mentioned above). In a recent multicenter, prospective, randomized, controlled trial (Guérin et al, 2013) investigators found that in patients with severe ARDS, early application of prone positioning was associated with significantly decreased 28-day and 90-day mortality. It’s really a little low-tech magic in the setting of high-tech interventions – keep it in your armamentarium to protect the fragile oxygenator.
References
Elmer J et al. Acute Respiratory Distress Syndrome After Spontaneous Intracerebral Hemorrhage. Crit Care Med. 2013; 41:1992–2001.
Guerin C et al. Prone Positioning in Severe Acute Respiratory Distress Syndrome. N Engl J Med. 2013;
368:2159-2168
Rosen DS, Macdonald RL. Subarachnoid Hemorrhage Grading Scales: A Systematic Review. Neurocrit Care.
2005;2:110–118.
This man has suffered a subarachnoid hemorrhage (SAH), which may or may not be associated with an aneurysm. Cocaine use causes abrupt large increases in blood pressure causing a rent in the arterial vasculature.
First a quick review: various scales are used to grade and prognosticate SAH, the most common of which are the Hunt and Hess scale and the World Federation of Neurological Surgeons (WFNS) scale. The Hunt and Hess scale is popular among emergency physicians for its ease of use and that it has been well studied:
Grade Neurologic status
1 Asymptomatic or mild headache and slight nuchal rigidity
2 Severe headache, stiff neck, no neurologic deficit except cranial nerve palsy
3 Drowsy or confused, mild focal neurologic deficit
4 Stuporous, moderate or severe hemiparesis
5 Coma, decerebrate posturing
Hunt and Hess grade 1 is associated with a 70% survival rate. Subsequent studies found similar survival rates between grades 1 and 2 (although this may have to do with problems of classification – the correlation
coefficient, κ, in a pooled analysis was 0.46, only moderate agreement). The key point here is that there is a
50% and higher mortality for grade 3 and above.
The WFNS scale offers the added advantage of incorporating GCS (arguably less subjective – κ in WFNS ranges from 0.27 to 0.6); however, it is more complicated and may be more difficult to remember:
Grade GCS score Motor deficit
1 15 Absent
2 13 to 14 Absent
3 13 to 14 Present
4 7 to 12 Present or absent
5 3 to 6 Present or absent
Some studies demonstrate that WFNS mortality steadily increases from grade 1 to grade 5, while others challenge its prognostic ability.
Our patient is experiencing neurogenic pulmonary edema (NPE), a type of non-cardiogenic pulmonary edema (i.e. a clinical diagnosis made by the presence of radiographic evidence of alveolar fluid accumulation without hemodynamic evidence to suggest a cardiogenic etiology – if measured, pulmonary artery wedge pressure ≤ 18 mmHg).
Neurogenic pulmonary edema may be caused by status epilepticus, head injury, or cerebral hemorrhage.
The pathophysiology of NPE is poorly understood. The theory is that a sympathetic surge from the medulla oblongata causes a neurologically mediated pulmonary venoconstriction, which increases the pulmonary capillary hydrostatic pressure and results in pulmonary edema.
It is important to distinguish non-cardiogenic pulmonary edema (here, the specific case of neurogenic
pulmonary edema) from cardiogenic pulmonary edema. Diuresis (B) would be a good choice for cardiogenic pulmonary edema due to volume overload, but may have untoward hemodynamic consequences in this setting of NPE. Although the presentation of acute respiratory distress syndrome (ARDS) may mimic NPE, ARDS protocols call for low tidal volumes and increasing PEEP (A) (i.e. rather than simply increasing the FiO2). Increasing PEEP in NPE should be used with extreme caution (and really only after an intracranial pressure monitor is placed), as it has been linked to decreased cerebral perfusion pressure and worsening outcomes (due to increased intrathoracic pressure, decreased venous return, systemic hypoperfusion).
Peak pressures may be elevated in lung parenchymal disease, especially if the plateau pressure is also elevated (as an aside, if the plateau pressure is normal and the peak pressure only is elevated, think airway obstruction). Unfortunately here, a slower respiratory rate (D) may inadvertently allow for hypercapnia, which would cause cerebral vasodilation and worsening intracranial pressure (perpetuating the vicious cycle of NPE). Further, slowing the respiratory rate (by increasing the expiratory time) is a strategy to improve auto-PEEP and breath-stacking (not to decrease the peak inspiratory pressure).
In distinction from other type of pulmonary edema, management of neurogenic pulmonary edema requires optimization of the primary neurologic insult and supportive care.
Prone positioning (C) is a tried-and-true adjunct to improve oxygenation in ventilated patients suffering
from a variety of pulmonary problems: dependent areas are better oxygenated. Also called the lung recruitment maneuver, prone positioning in mechanically ventilated patients optimizes functional residual capacity, redistributes blood flow (minimizes V-Q mismatch), aids in diaphragm excursion, and improves secretion removal. It is a natural way to improve oxygenation and ventilation without untoward physiologic consequences (as mentioned above). In a recent multicenter, prospective, randomized, controlled trial (Guérin et al, 2013) investigators found that in patients with severe ARDS, early application of prone positioning was associated with significantly decreased 28-day and 90-day mortality. It’s really a little low-tech magic in the setting of high-tech interventions – keep it in your armamentarium to protect the fragile oxygenator.
References
Elmer J et al. Acute Respiratory Distress Syndrome After Spontaneous Intracerebral Hemorrhage. Crit Care Med. 2013; 41:1992–2001.
Guerin C et al. Prone Positioning in Severe Acute Respiratory Distress Syndrome. N Engl J Med. 2013;
368:2159-2168
Rosen DS, Macdonald RL. Subarachnoid Hemorrhage Grading Scales: A Systematic Review. Neurocrit Care.
2005;2:110–118.