Neuropsychiatrie de l'Enfance et de l'Adolescence

Darmon M., Schnell D., Zeni F.

Renal sonography is performed routinely to assess renal and collecting system morphology. B-mode sonography provides valuable information on anatomic features including kidney size (longitudinal diameter and parenchyma thickness) and appearance (kidney margins and echogenicity of the parenchyma, cortex, medulla, and papillae); presence and degree of hydronephrosis; and presence of stones, calcification, cysts, or solid masses. However, B-mode sonography does not evaluate kidney function. Renal Doppler, in contrast, helps to assess renal perfusion and renal function of native or transplanted kidneys (Fig. 1). Renal Doppler is valuable for assessing large arterial or venous abnormalities and has been suggested for evaluating changes in intrarenal perfusion due to diseases of the renal parenchyma [1–5]. The Doppler-based renal resistive index is a recently suggested tool for assessing changes in renal perfusion in critically ill patients [6–8] and for predicting acute kidney injury (AKI) in patients with severe sepsis [9]. However, many factors influence the renal resistive index and should be taken into account when interpreting resistive index values in critically ill patients [10].

Malbrain M.L., De Laet I., De Waele J.

A compartment syndrome exists when the increased pressure in a closed anatomic space threatens the viability of enclosed and surrounding tissue [1]. Within the body there are four major compartments: The head, the chest, the abdomen, and the extremities. Within each compartment an individual organ or a region with multiple organs can be affected by a compartment syndrome. Table 1 summarizes the different compartments and their related pathologies [2]. A compartment syndrome is not a disease; as such it can have many causes and can develop within many disease processes.

Degos V., Lescot T., Puybasset L.

An uncontrolled increase in intracranial pressure (ICP), often due to cerebral edema, is the most common cause of death in patients with traumatic brain injury (TBI). Different types of edema coexist in TBI patients: Vasogenic edema and cytotoxic edema. Vasogenic edema occurs with the extravasation of fluid into the extracellular space following blood brain barrier (BBB) disruption. Cytotoxic edema results from a shift of water from the extracellular compartment into the intracellular compartment due, in part, to alterations in normal ionic gradients. Description of the localization and knowledge of the chronology, determinants, and kinetics of the BBB disruption are necessary to adapt therapeutic strategy.

Werdan K., Russ M., Buerke M.

What can we expect from the implementation of an intra-aortic balloon counterpulsation pump (IABP) in a patient with shock (Fig. 1)? The conventional indication for IABP is cardiogenic shock of ischemic etiology. With the IABP in place in the thoracic aorta, inflation of the balloon in diastole and active deflation in systole induces higher perfusion pressures in the brain and the coronary arteries in diastole and unloads the diseased heart by reducing left ventricular afterload in systole. Of special relevance is the volume shifting of about 40 ml per beat by the IABP, increasing left ventricular ejection fraction and thereby cardiac output in the range of at best 1 l/min.

Solaiman O., Zygun D.

Acute traumatic spinal cord injury primarily afflicts young people and significantly reduces independence, bestows life-long disability, and consumes huge societal resources. The estimated incidence of acute traumatic spinal cord injury in North America varies from 27–81 cases per million inhabitants per year [1]. The prevalences of spinal cord injury were estimated to be 280 and 681 individuals per million inhabitants in Finland and Australia, respectively. Despite recent efforts at prevention, including laws mandating seat belt use, the incidence of spinal cord injury has not changed significantly andmay actually be increasing in certain parts of the population [2, 3]. In addition, the estimated (2006) treatment cost of spinal cord injury is $9.7 billion per year [1]. A number of pharmacological agents (methylprednisolone sodium succinate, and the related compound, tirilazad mesylate; GM-1 ganglio-side; thyrotropin-releasing hormone; gacyclidine; naloxone; and nimodipine) have been investigated in large, prospective, randomized, controlled clinical trials, but all have failed to demonstrate convincing neurological benefit. Spinal cord injury is frequently associated with systemic hypotension attributable to hypovolemia, direct spinal cord trauma, or both [4].

Nguyen Y.-., Mayr F.B., Angus D.C.

Advances in medical science and health care have gradually changed the nature of dying. Death no longer is likely to be the sudden result of infection or injury, but instead occurs slowly, in old age, and at the end of a period of life-limiting or chronic illness. This shift has created new challenges for critical care medicine. In this chapter, we provide a brief overview about critical care utilization at the end-of-life and the most important challenges we face. We discuss these challenges from an American and European perspective, as end-of-life decisions vary substantially between these two continents.

Frasca D., Dahyot-Fizelier C., Mimoz O.

In the USA, more than five million patients require central venous access each year. Unfortunately, central venous access can be associated with adverse events that are hazardous to patients and expensive to treat. Infection remains the main complication of intravascular catheters in critically ill patients. Catheter-related bloodstream infections have been reported to occur in 3 to 8 % of inserted catheters and are the first cause of nosocomial bloodstream infection in intensive care units (ICUs), with 80,000 cases annually at a cost of $300 million to $2.3 billon [1]. Additional financial costs may be as high as $30,000 per survivor, including one extra week in the ICU and two to three additional weeks in the hospital. Attributable mortality rates range from 0 to 35 %, depending on the degree of control for severity of illness.

Ruiz C., Hernandez G., Ince C.

Shock has typically been classified into four types: Hypovolemic, cardiogenic, obstructive, and distributive. The first three categories are associated with a decrease in cardiac output, leading to tissue hypoxia. Distributive shock, such as septic shock, results from abnormal distribution of normal or increased cardiac output, secondary to microcirculatory dysfunction. Severe disruption of the microcirculation during sepsis results in a pathologic heterogeneity in microvascular blood flow that occurs as a consequence of the shutdown of weak microcirculatory units. This implies that oxygen transport is shunted from the arterial to the venous compartment, leaving the microcirculation hypoxic, and is the main pathogenic feature of distributive shock. Such a scenario results in maldistribution of microvascular blood flow and a mismatch between oxygen delivery and oxygen demand in different tissues that seems to be the first step in the progression to organ failure [1].

Boyd J.H.

Nearly all critically ill patients requiring advanced life support exhibit systemic inflammation. Septic shock, the most common disorder in the critically ill, results from the direct adverse consequences of infection combined with a maladaptive response resulting in fulminant systemic inflammation. This powerful interaction results in a mortality rate of up to 50 % for victims of this disease [1–4]. While septic shock is most often described as ‘warm’ hypotension (particularly lowering diastolic blood pressure) despite initial resuscitation, the patient often exhibits circulatory failure demonstrated by mottled extremities and low mixed or central venous oxygen saturation as a result of inadequate oxygen delivery. A key component of the shock due to severe sepsis, cardiac impairment, can be demonstrated in 50–100 % of patients diagnosed with septic shock [5–9]. While diagnosed at the macrovascular level, cardiac pump failure is itself due to microcirculatory dysfunction and impaired oxygen extraction in the heart [10]. A daily clinical challenge faced by those caring for the critically ill is that while the patient presents with circulatory failure, advanced studies such as echocardiography and measurement of central venous oxygen tension (ScvO2) actually demonstrate normal or even supra-normal cardiac output. This picture is often accompanied by an increasing lactate level and progressive organ dysfunction. It is now believed that this failure to adequately perfuse vital organs despite an ostensibly normal macrocirculation is due to dysfunction of the microcirculation.

Brindley P.G.

It is estimated that approximately 40,000–100,000 Americans die annually from medical errors [2]. Thousands more suffer harm from medical errors. Still others are exposed to errors, but are lucky enough to suffer no obvious harm [3]. In fact, medical errors are now the eighth leading cause of death in the USA; data are no less alarming from other nations [4]. Regardless of the exact figures, it seems that patient safety is far from adequate. Crudely put, if medicine were a patient, we physicians would say it is time to admit there is a problem. We would expect urgent action, and we would welcome any ideas, rather than tolerate further delays. This chapter hopes to provide a call-to-arms, but most importantly a range of ideas, both new and old, to achieve the sort of care that our patients deserve.

Roppolo L.P., Pepe P.E., Bobrow B.J.

Gasping is a physiologic entity that, among other conditions, is seen typically in mammals who have sustained a global ischemic insult such as sudden cardiac arrest or severe hemorrhagic shock [1–13]. Scientists have defined a gasp formally in nomenclature consensus processes as “an abrupt, sudden, transient inspiratory effort” [13] and it has been described in the published literature since 1812 [11]. The classic gasping that occurs after sudden cardiac arrest is also sometimes referred to as “agonal breaths” or “agonal respirations” [1, 3–6, 9]. However, the term agonal breathing may also be used by some when referring to a broader variety of respiratory efforts or conditions [12, 14]. Agonal breathing may, therefore, refer to various kinds of abnormal breathing observed at the time of clinical death, during certain types of stroke, or in progressive respiratory failure when rapid breathing reverts to slower and often shallow breaths [6, 11, 12, 14]. Classic gasps, according to strict definition, however, are usually sudden, abrupt, and much brisker and larger than normal respiratory efforts [13].

De Corte W., De Laet I., Hoste E.A.

Acute kidney injury (AKI) defined by the sensitive Risk, Injury, Failure, Loss, and End-stage kidney disease (RIFLE) or AKI criteria occurs in 10 to 60 % of intensive care unit (ICU) patients, and is associated with increased mortality [1, 2]. Despite advances in ICU care, the mortality of patients with AKI has remained more or less stable over recent years [3]. A possible explanation for this unchanged mortality in AKI includes the plethora of definitions used to define AKI, but also differences in case mix, including more older and more seriously ill patients.

Luepschen H., Leonhardt S., Putensen C.

Electrical impedance tomography (EIT) of the lungs is a bedside-available, noninvasive, and radiation-free medical imaging modality which allows real-time imaging of electrical impedance (i.e., resistance to alternating currents) changes in the thorax [1]. During breathing, lung tissue, with its relatively high impedance oscillations, is the main contributor to these changes which has led to a multitude of applications in monitoring regional lung ventilation [2–5, for review see 6, 7].

Leppäniemi A.K.

Laparostomy is a surgical treatment method in which the peritoneal cavity is opened anteriorly and deliberately left open, hence often called ‘open abdomen’. The abdominal contents are exposed and protected with a temporary coverage. The term does not include full-thickness abdominal wall defects resulting from partial excision due to tumor or necrotizing infection, or incisional hernias.

Moreno R.P., Metnitz P., Bauer P.

The use of all-cause hospital mortality as the sole or major endpoint for the evaluation of clinical trials in intensive care was challenged in the mid 1980s, in the aftermath of a very long series of negative clinical trials in patients with sepsis, severe sepsis, and septic shock [1]. This outcome measure, until then viewed as the golden standard in clinical trials in intensive care, is, beyond any doubt, a very relevant endpoint both for researchers and for clinicians. Its use has been contested because hospital policy can and does change the location of deaths (e.g., discharging patients to the ward to die) and mortality rates can, therefore, be significantly underestimated in hospitals that discharge patients very early in the course of their disease to other facilities [2].