Principles of Brain Management: 1

One critical thread of research on the social brain starts with the “threat and he calls it “the fundamental organizing principle of the brain.
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There are two main classes of environment signals you want to seek:. Customer signals are the qualitative and quantitative data sets you accumulate on how customers are using the product.

Intracranial pressure

They are the changes in the competitive, political, and socioeconomic landscapes that affect your company and customers. Constantly listening to the world outside your company walls is a critical input to great product management. And what you hear from customers is the ultimate validation of your achievement of the goal.

How far a rocket ship can go is constrained by the fuel it holds, the quality of its crew, and its time-constrained ability to leverage gravitational boosts using from other celestial bodies like Jupiter. Similarly, product teams are constrained by the money, people, and time they have to launch a product. On any given mission, a product team will be constrained by all three of these. People on a product team often represent the biggest constraint.

Too often, that constraint is only thought of as the number of people working on a product which it can be , but vastly more important are actual skill and experience levels of the people on the team. To be clear, this applies to the PMs themselves, as well. Money is a constraint that relates to the ability of a team to hire the right people salaries , enable them to work overhead like office space , operate the product servers and support , and distribute it marketing. It would be silly to spend all of your money on salaries to hire the best team, but then not have an office for them to work in, or not have a single dollar to pay for marketing and thus very few customers will find the product.

In lieu of these luxuries, PMs need to consider all the money impacts when building their strategy. PMs must manage time. When PMs know the goal, understand the environment, and respect the constraints, they have the necessary inputs to build a great product strategy, which sits somewhere in the intersection of those inputs. My reductionist analogy may imply this is easy, but let me be clear that forming a good strategy is very, very difficult.

In fact, despite being confident enough to write this post, I am not confident that I can always find the right strategy in practice. The other dimension that I hope comes through from this section is that PMs need incredible breadth to effectively synthesize these inputs into strategy. Knowing enough about engineering, UX, data, finance, organizational design, operations, research, marketing, etc.

I really think this type of thinking is counterproductive, and will limit your potential. As scary as it sounds, it is important that you try to learn everything. Temper the fear that comes with this with the acknowledgement that, at the same time, it is impossible to know it all. In the rocket ship analogy, who did you think the PM was? Were they the person who planted the flag on planet Goal, or were they one of the astronauts on the ship? The answer is neither. There is no better analogy for how a PM should think of their role than the coach of a team sport like basketball, volleyball, football, etc.

They are hired to support a team, and do so by helping them increase their individual and collective potentials. They are measured - by the team and owners alike - by winning. We do this by enabling the team to maximize their individual and collective potentials by aligning everyone on a product strategy principle A and fostering a healthy team dynamic.

When I first wrote that PMs are like sports coaches, what did you visualize? Do you see the coach as a parent and the team as kids? Or are the players like Lebron, telling the coach what to do? How about the wrist wrapping assistant coaches? PMs need strong self awareness to recognize when to lead, partner, or support their team.

I will prescribe the frameworks, goals, and even how to organize the execution of the project. To be clear, a PM should aspire to collaborate in all cases, but this relative-skill dynamic warrants it the most. I will ask, how can I be helpful? For example, I will start by asking the experienced team about their vision, and then follow it up with lots of questions to get down to their first principles and strategy.

I can still do my job.

Note that in all cases, the PM is still responsible for the development of the product strategy, but how they get there can be very different. Without a doubt, not understanding this dynamic of relative skill between the team and the PM, is the number one reason that PMs fail. They misread the situation, fall into the trap of thinking PM equals mini-CEO by default, and immediately lose trust with their team, which takes ten times as long to win back. People rarely talk about the coach when a team wins. The same should be true for product teams.

You need to have empathy and respect for all the work individuals on your team undertake. Significant risk factors for later seizures are brain contusions, subdural hematoma, depressed skull fracture, penetrating head wound, loss of consciousness or amnesia for more than 1 day, and age 65 years or older.

In a randomized clinical trial, phenytoin reduced the incidence of seizures during the first week after trauma, but not thereafter [ 43 ]. Based on this study, seizure prophylaxis for patients with severe brain injury is recommended for the first 7 days after injury. Treatment with anticonvulsants beyond 7 days should be reserved for patients who develop late seizures [ 44 ].

Emergent surgical management should be considered whenever intracranial hypertension occurs suddenly or is refractory to medical management. Routine paralysis of patients with neurosurgical disorders is not indicated; however, intracranial hypertension caused by agitation, posturing, or coughing can be prevented by sedation and nondepolarizing muscle relaxants that do not alter cerebrovascular resistance [ 45 ]. Although a disadvantage of this therapy is that the neurologic examination cannot be monitored closely, the sedatives and muscle relaxants can be interrupted once a day, usually before morning rounds, to allow neurologic assessments.

Major complications of neuromuscular blockade are myopathy, polyneuropathy, and prolonged neuromuscular blockade. Myopathy is associated with the use of neuromuscular blocking agents, particularly in combination with corticosteroids [ 46 ]. Polyneuropathy has been observed in patients with sepsis and multiple organ failure. Prolonged neuromuscular blockade is seen in patients with multiple organ failure especially with kidney and liver dysfunction.

Recommendations to minimize these complications are limiting the use and dose of neuromuscular blocking agents, train-of-four monitoring, measuring creatine phosphokinase daily, and stopping the drug daily to evaluate motor response [ 47 ]. Mannitol is the most commonly used hyperosmolar agent for the treatment of intracranial hypertension. More recently, hypertonic saline also has been used in this circumstance.

A few studies have compared the relative effectiveness of these two hyperosmotic agents, but more work is needed. Intravenous bolus administration of mannitol lowers the ICP in 1 to 5 minutes with a peak effect at 20 to 60 minutes. The effect of mannitol on ICP lasts 1. Mannitol usually is given as a bolus of 0. Two prospective clinical trials, one in patients with subdural hematoma and the other in patients who have herniated from diffuse brain swelling, have suggested that a higher dose of mannitol 1.

When long-term reduction of ICP is needed, 0. Mannitol has rheologic and osmotic effects. Immediately after infusion of mannitol, there is an expansion of plasma volume and a reduction in hematocrit and in blood viscosity, which may increase CBF and on balance increase oxygen delivery to the brain. These rheologic effects of mannitol depend on the status of pressure autoregulation [ 51 ].

In patients with intact pressure autoregulation, infusion of mannitol induces cerebral vasoconstriction, which maintains CBF constant, and the decrease in ICP is large. In patients with absent pressure autoregulation, infusion of mannitol increases CBF, and the decrease in ICP is less pronounced. Mannitol also may improve microcirculatory rheology [ 50 ] and has free radical scavenging effects.

The osmotic effect of mannitol increases serum tonicity, which draws edema fluid from cerebral parenchyma. This process takes 15 to 30 minutes until gradients are established. Serum osmolarity seems to be optimal when increased to to mOsm and should be kept at less than mOsm to avoid side effects of therapy, such as hypovolemia, hyperosmolarity, and renal failure. Mannitol opens the blood-brain barrier, and mannitol that has crossed the blood-brain barrier may draw fluid into the central nervous system, which can aggravate vasogenic edema.

For this reason, when it is time to stop mannitol, it should be tapered to prevent a rebound in cerebral edema and ICP. The adverse effects of mannitol are most likely when mannitol is present in the circulation for extended periods, such as in slow or continuous infusions or with repeated administration of higher than necessary doses. In some studies, hypertonic saline has been more effective at reducing ICP than mannitol [ 52 , 53 ]. Hypertonic saline has a clear advantage over mannitol in hypovolemic and hypotensive patients. Mannitol is relatively contraindicated in hypovolemic patients because of the diuretic effects, whereas hypertonic saline augments intravascular volume and may increase blood pressure in addition to decreasing ICP.

Hypertonic saline was not associated with improved neurologic outcomes, however, when given as a prehospital bolus to hypotensive patients with severe TBI [ 54 ]. Adverse effects of hypertonic saline administration include hematologic and electrolyte abnormalities, such as bleeding secondary to decreased platelet aggregation and prolonged coagulation times, hypokalemia, and hyperchloremic acidosis [ 55 ]. Hyponatremia should be excluded before administering hypertonic saline to reduce the risk of central pontine myelinolysis.

The resulting reduction in cerebral blood volume decreases ICP. Hyperventilation has limited use in the management of intracranial hypertension, however, because this effect on ICP is time limited, and because hyperventilation may produce a sufficient decrease in CBF to induce ischemia. The vasoconstrictive effect on cerebral arterioles lasts only 11 to 20 hours because the pH of the CSF rapidly equilibrates to the new PaCO 2 level.

As the CSF pH equilibrates, the cerebral arterioles redilate, possibly to a larger caliber than at baseline, and the initial reduction in cerebral blood volume comes at the cost of a possible rebound phase of increased ICP [ 57 , 58 ]. For this reason, the most effective use of hyperventilation is acutely to allow time for other, more definitive treatments to be put into action. When hypocarbia is induced and maintained for several hours, it should be reversed slowly, over several days, to minimize this rebound hyperemia [ 59 ].

Hyperventilation decreases CBF, but whether this reduction in flow is sufficient to induce ischemia in injured brain is controversial. Although hyperventilation-induced ischemia has not been clearly shown, routine chronic hyperventilation to PaCO 2 of 20—25 mm Hg had a detrimental effect on outcome in one randomized clinical trial [ 59 ]. The authors of this study recommended using hyperventilation only in patients with intracranial hypertension, rather than as a routine in all head-injured patients.

This view is reinforced in TBI guidelines. Barbiturate coma should only be considered for patients with refractory intracranial hypertension because of the serious complications associated with high-dose barbiturates, and because the neurologic examination becomes unavailable for several days [ 62 ]. Although routine use of barbiturates in unselected patients has not been consistently effective in reducing morbidity or mortality after severe head injury [ 63 , 64 ], a randomized multicenter trial showed that instituting barbiturate coma in patients with refractory intracranial hypertension resulted in a twofold greater chance of controlling the ICP [ 65 ].

Studies by Messeter and colleagues [ 66 , 67 ] have suggested that the reduction in ICP with barbiturates is closely tied to the retention of carbon dioxide reactivity by the brain. Hypotension caused by pentobarbital should be treated first with volume replacement and then with vasopressors if necessary. Experimental studies suggest that for the treatment of hypotension associated with barbiturate coma, volume resuscitation may be better than dopamine [ 69 ] because dopamine infusion increased cerebral metabolic requirements and partially offset the beneficial effects of barbiturates on CMRO 2.

Although a multicenter randomized clinical trial of moderate hypothermia in severe TBI did not show a beneficial effect on neurologic outcome, it was noted that fewer patients randomized to moderate hypothermia had intracranial hypertension [ 70 ].

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A pilot randomized clinical trial of hypothermia in children with TBI produced similar findings—no improvement in neurologic outcome, but a reduction in ICP during the hypothermia treatment [ 71 ]. Although routine induction of hypothermia is not indicated at present, hypothermia may be an effective adjunctive treatment for increased ICP refractory to other medical management. Steroids commonly are used for primary and metastastic brain tumors, to decrease vasogenic cerebral edema.

Focal neurologic signs and decreased mental status owing to surrounding edema typically begin to improve within hours [ 72 ]. Increased ICP, when present, decreases over the following 2 to 5 days, in some cases to normal. The most commonly used regimen is intravenous dexamethasone, 4 mg every 6 hours. For other neurosurgical disorders, such as TBI or spontaneous intracerebral hemorrhage, steroids have not been shown to have a benefit [ 73 , 74 ] and in some studies have had a detrimental effect [ 75 , 76 ].

Administration of methylprednisolone resulted in a significant increase in the risk of death from This trial confirmed previous studies and guidelines that routine administration of steroids is not indicated for patients with TBI. Intracranial masses producing elevated ICP should be removed when possible.

Acute epidural and subdural hematomas are a hyperacute surgical emergency, especially epidural hematoma because the bleeding is under arterial pressure. Brain abscess must be drained, and pneumocephalus must be evacuated if it is under sufficient tension to increase ICP. Surgical management of spontaneous intracerebral bleeding is controversial [ 77 ].

CSF drainage lowers ICP immediately by reducing intracranial volume and more long-term by allowing edema fluid to drain into the ventricular system. Drainage of even a small volume of CSF can lower ICP significantly, especially when intracranial compliance is reduced by injury. This modality can be an important adjunct therapy for lowering ICP. If the brain is diffusely swollen, the ventricles may collapse, and this modality then has limited utility. The surgical removal of part of the calvaria to create a window in the cranial vault is the most radical intervention for intracranial hypertension, negating the Monro-Kellie doctrine of fixed intracranial volume and allowing for herniation of swollen brain through the bone window to relieve pressure.

Decompressive craniectomy has been used to treat uncontrolled intracranial hypertension of various origins, including cerebral infarction [ 78 ], trauma, subarachnoid hemorrhage, and spontaneous hemorrhage. Patient selection, timing of operation, type of surgery, and severity of clinical and radiologic brain injury all are factors that determine the outcome of this procedure.

Sahuquillo and Arikan [ 79 ] reviewed the evidence in the literature for studies evaluating the effectiveness of decompressive craniectomy after TBI. They found only one small randomized clinical trial in 27 children with TBI [ 80 ]. This trial found a reduced risk ratio for death of 0. All of the available studies in adults are either case series or cohorts with historical controls. Brain oxygenation measured by tissue PO 2 and blood flow estimated by middle cerebral artery flow velocity also are usually improved after decompressive craniectomy [ 83 , 84 ].

Reported complications include hydrocephalus, hemorrhagic swelling ipsilateral to the craniectomy site, and subdural hygroma [ 81 ]. A case report of paradoxical herniation also has been reported after a lumbar puncture in a patient with a decompressive craniectomy [ 85 ]. There are limited results from randomized trials to confirm or refute the effectiveness of decompressive craniectomy in adults. Reports suggest, however, that decompressive craniectomy may be a useful option when maximal medical treatment has failed to control ICP.

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In a pooled analysis of randomized trials in patients with malignant MCA infarction, decompressive surgery undertaken within 48 h of stroke was associated with reduced mortality and an increased proportion of patients with a favourable functional outcome [ 87 ]. Effective treatment of intracranial hypertension involves meticulous avoidance of factors that precipitate or aggravate increased ICP.

When ICP becomes elevated, it is important to rule out new mass lesions that should be surgically evacuated. Medical management of increased ICP should include sedation, drainage of CSF, and osmotherapy with either mannitol or hypertonic saline. Steroids are not indicated and may be harmful in the treatment of intracranial hypertension resulting from TBI. PMC documents will be made available for review after conversion approx. Any corrections that need to be made will be done at that time.

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Abstract Effective management of intracranial hypertension involves meticulous avoidance of factors that precipitate or aggravate increased intracranial pressure. Intracranial pressure Normal values In normal individuals with closed cranial fontanelles, central nervous system contents, including brain, spinal cord, blood, and cerebrospinal fluid CSF , are encased in a noncompliant skull and vertebral canal, constituting a nearly incompressible system.

Intracranial hypertension Causes of intracranial hypertension The different causes of intracranial hypertension Box 1 can occur individually or in various combinations. Causes of intracranial hypertension Intracranial primary. Intracranial hypertension secondary to traumatic brain injury Special features should be considered in patients with traumatic brain injury TBI , in which lesions may be heterogeneous, and several factors often contribute to increase the ICP [ 12 ]: Cerebral edema [ 13 ].


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Hyperemia owing to vasomotor paralysis or loss of autoregulation [ 14 ]. Increased intrathoracic or intra-abdominal pressure as a result of mechanical ventilation, posturing, agitation, or Valsalva maneuvers. Neurologic intensive care monitoring Intracranial hypertension is an important cause of secondary injury in patients with acute neurologic and neurosurgical disorders and typically mandates specific monitoring. Intracranial pressure monitoring Clinical symptoms of increased ICP, such as headache, nausea, and vomiting, are impossible to elicit in comatose patients.

Types of monitors The ventriculostomy catheter is the preferred device for monitoring ICP and the standard against which all newer monitors are compared [ 20 ]. Types of intracranial pressure waveforms The variations seen in the normal tracing of ICP originate from small pulsations transmitted from the systemic blood pressure to the intracranial cavity. Pathologic waveforms As the ICP increases, cerebral compliance decreases, arterial pulses become more pronounced, and venous components disappear.

Indications for intracranial pressure monitoring Monitoring of ICP is an invasive technique and has some associated risks. Intracranial pressure treatment measures: Open in a separate window.


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  5. Management of Intracranial Hypertension!

Diagram of diagnosis and treatment of intracranial hypertension. General care to minimize intracranial hypertension Prevention or treatment of factors that may aggravate or precipitate intracranial hypertension is a cornerstone of neurologic critical care. Optimizing cerebral venous outflow To minimize venous outflow resistance and promote displacement of CSF from the intracranial compartment to the spinal compartment, elevation of the head of the bed and keeping the head in a neutral position are standards in neurosurgical care. Respiratory failure Respiratory dysfunction is common in patients with intracranial hypertension, especially when the cause is head trauma.

Sedation and analgesia Agitation and pain may significantly increase blood pressure and ICP. Hypertension Elevated blood pressure is seen commonly in patients with intracranial hypertension, especially secondary to head injury, and is characterized by a systolic blood pressure increase greater than diastolic increase. Treatment of anemia Anecdotal cases have been reported of patients with severe anemia presenting with symptoms of increased ICP and signs of papilledema, which resolve with treatment of the anemia [ 39 ].

Measures for refractory intracranial hypertension For patients with sustained ICP elevations of greater than 20 to 25 mm Hg, additional measures are needed to control the ICP. Medical interventions Heavy sedation and paralysis Routine paralysis of patients with neurosurgical disorders is not indicated; however, intracranial hypertension caused by agitation, posturing, or coughing can be prevented by sedation and nondepolarizing muscle relaxants that do not alter cerebrovascular resistance [ 45 ]. Hyperosmolar therapy Mannitol is the most commonly used hyperosmolar agent for the treatment of intracranial hypertension.

Barbiturate coma Barbiturate coma should only be considered for patients with refractory intracranial hypertension because of the serious complications associated with high-dose barbiturates, and because the neurologic examination becomes unavailable for several days [ 62 ]. Hypothermia Although a multicenter randomized clinical trial of moderate hypothermia in severe TBI did not show a beneficial effect on neurologic outcome, it was noted that fewer patients randomized to moderate hypothermia had intracranial hypertension [ 70 ].

Steroids Steroids commonly are used for primary and metastastic brain tumors, to decrease vasogenic cerebral edema. Surgical interventions Resection of mass lesions Intracranial masses producing elevated ICP should be removed when possible. Cerebrospinal fluid drainage CSF drainage lowers ICP immediately by reducing intracranial volume and more long-term by allowing edema fluid to drain into the ventricular system.

Decompressive craniectomy The surgical removal of part of the calvaria to create a window in the cranial vault is the most radical intervention for intracranial hypertension, negating the Monro-Kellie doctrine of fixed intracranial volume and allowing for herniation of swollen brain through the bone window to relieve pressure.

Management of Intracranial Hypertension

Summary Effective treatment of intracranial hypertension involves meticulous avoidance of factors that precipitate or aggravate increased ICP. Volume regulation of the brain tissue—a survey. Acta Neurochir Wien ; Cerebral vasomotor paralysis produced by intracranial hypertension. The intracranial pressure in infants.

The effect of intracerebral hematoma location on the risk of brain stem compression and on clinical outcome. Prediction of a response in ICP to induced hypertension using dynamic testing of cerebral pressure autoregulation. Cerebral perfusion pressure, intracranial pressure, and head elevation. The relation between intracranial pressure, mean arterial pressure and cerebral blood flow in patients with severe head injury. Medication-induced intracranial hypertension in dermatology.

Am J Clin Dermatol. Jacob S, Rajabally YA. Intracranial hypertension induced by rofecoxib. Digre K, Warner J. Is vitamin A implicated in the pathophysiology of increased intracranial pressure? Guidelines for the acute medical management of severe traumatic brain injury in infants, children, and adolescents: Pediatr Crit Care Med.

A new therapy of post-trauma brain oedema based on haemodynamic principles for brain volume regulation. Diffuse cerebral swelling following head injuries in children: Contribution of edema and cerebral blood volume to traumatic brain swelling in head-injured patients. Long-term observations of intracranial pressure after severe head injury: Traumatic subarachnoid hemorrhage as a predictable indicator of delayed ischemic symptoms. Papilledema after acute head injury.

Significance of CT in head injury: Chapter 7 intracranial pressure monitoring technology. Clinical evaluation of a miniature strain-gauge transducer for monitoring intracranial pressure. Laboratory testing of three intracranial pressure microtransducers: Continuous recording and control of ventricular fluid pressure in neurosurgical practice. Role of intracranial pressure monitoring in severely head-injured patients without signs of intracranial hypertension on initial computerized tomography.

N Engl J Med. Risk of Infection with Prolonged Ventricular Catheterization. Efficacy of antimicrobial-impregnated external ventricular drain catheters: Effect of head elevation on intracranial pressure, cerebral perfusion pressure, and cerebral blood flow in head-injured patients. Effects of head posture on cerebral hemodynamics: Decompressive laparotomy to treat intractable intracranial hypertension after traumatic brain injury.

North JB, Jennett S. Abnormal breathing patterns associated with acute brain damage. Secondary insults to the injured brain. J R Coll Surg Edinb.