Radiation ulcers are wounds caused by the acute or chronic effects of ionizing radiation. The injury may involve the skin, underlying soft tissue, and even deep structures such as bone. The most common cause of radiation injury is an adverse effect of therapeutic radiation therapy. Other causes are occupational or environmental exposures.
History of the Procedure
Wilhelm Konrad Roentgen discovered X-rays in 1895. The realization that radiation can cause tissue injury followed shortly thereafter. Many different forms of radiation have since been discovered, and applications have been developed for medical, industrial, and military use.
The common pathway of radiation injury to tissue, regardless of the source of the radiation, is interaction of the radiation energy with DNA that causes structural damage to the DNA. Depending on the precise area of injury in the cell, the damage may be repaired, cause cell death, or cause delayed effects. This damage can lead to both acute and chronic tissue effects.
Problem
Ionizing radiation may come from high-energy photons that can be the product of natural decay of radioactive material, such as gamma rays, or the product of artificial bombardment of electrons onto Tungsten, such as X-rays. Gamma rays and X-rays can be manipulated to control the amount of energy and the depth of penetration. The energy delivered to the tissues is measured in electron volts. Orthovoltage radiation is used in therapeutic radiation, and includes radiation at 80-400 keV. Supervoltage radiation delivers energy in excess of 1 million V.
Radiation can also be produced by high energy particles that are a product of radioactive decay. Alpha particles are helium nuclei emitted by various elements, including radium. Alpha particles penetrate poorly but can be taken up in local tissues. Beta particles are electrons. They penetrate the skin superficially and can be useful in treating relatively superficial skin conditions, such as mycosis fungoides.
Brachytherapy is radiation therapy delivered with a short distance between the radiation source and the target. Many radioactive isotopes are used, such as iodine-125, gold-198, and cesium-137. Needles filled with radioactive seeds, mechanical appliances, permanent seeds, and other modalities can be used.
Radiation delivery is measured by the amount of radiation absorbed by a gram of tissue. One rad is equal to 100 ergs of energy absorbed per gram of tissue. The most common unit of measurement is the gray, which is equal to 100 rad.
Frequency
The true incidence of radiation injury to normal tissue is unknown. An acceptable short-term complication rate from radiation therapy is in the range of 5-15%. The long-term complication rate is unknown and, of course, affected by long-term survival rate. As cancer therapy becomes increasingly effective, patients are living long enough to have the adverse late effects of their radiation treatment.
Etiology
The acute effect of ionizing radiation is direct cell damage to DNA. This damage may cause immediate cell death, prevent proliferating cells from dividing, or induce apoptosis. The late effect is fibrosis. The mechanism of fibrosis production is unclear, but it may involve proinflammatory and profibrotic cytokines, such as tumor necrosis factor-alpha. The fibrosis is progressive.
Pathophysiology
Tissues affected by acute high-dose radiation, as in industrial accidents, manifest progressive obliterative endarteritis culminating in tissue necrosis. Long-term radiation injury results in fibrosis of the dermal and subcutaneous tissues. Elastin fibers are fragmented. The skin loses its rete pegs. The number of blood vessels may be normal; however, fibrosis around them impairs their ability to contract. Electron microscopy may show dehiscence of endothelial cells and microthrombi.
Radiation damage to cells can also lead to future malignancies. These may arise in chronic wounds due to radiation damage. They can also be the cause of nonhealing wounds.
On a cellular level, radiation-induced damage can be direct or indirect. Direct damage results from the hits to, or radiation absorption by, the cells. In contrast, indirect damage occurs when the radiation causes cellular water to release free radicals, which in turn combine to make cytotoxic peroxides. Direct effects of radiation can affect cellular DNA, which, when altered, may lead to cellular destruction or aberrant cellular replication and malignancy.
These direct and indirect cellular alterations also occur at the level of the fibroblast. In the development of soft tissue wounds and ulcerations in irradiated fields, extensive research implicates fibroblast dysfunction and depletion as culprits because of decreased collagen deposition in soft tissues. Although most investigators agree that vascular injury also inhibits wound healing, Rudolph et al question this notion (1982). They suggest that oxygen tension is not altered in irradiated tissues compared with nonirradiated fields and that the onus of impaired wound healing falls on this fibroblast dysfunction.
Clinical
The 3 types of radiation injury are acute, subacute, and chronic.
Acute injury refers to radiation exposure that often occurs in a setting such as an industrial accident. It is usually caused by orthovoltage radiation in the range of 5000-10,000 rads. The effects on the skin and exposed soft tissues are like those of a thermal burn, with alterations and destruction of the basal cells of the epidermis, though these effects are slower and more progressive than those due to thermal burns. Erythema results and may be recurrent. Along with erythema, the patient has pain, edema, itching, and eventual desquamation of the skin. This desquamation can progress to soft tissue necrosis and obliterative endarteritis. Superimposed infection also may complicate the clinical course.
Subacute injury differs from the acute form in that it is caused by recurrent exposures to radiation over time, as with therapeutic radiation. This type of radiation tends to be of lower energy than that observed in occupational or environmental exposures. It also causes cutaneous erythema and edema, but the erythema tends to be transient and necrosis is usually absent. Another characteristic finding after multiple radiation treatments is hyperpigmentation and a woody induration of the soft tissues. In terms of vascular effects, studies have demonstrated the following changes in irradiated vessels: decreased smooth muscle; increased collagen levels with fibrosis and thickening of the walls; hyaline degeneration and breakdown of elastic lamina; dehiscence of endothelial cells; and fibrinoid necrosis and microthrombi in the lumina leading to ineffective delivery of oxygen, other vital nutrients, and antibiotics.
Chronic injury results from long-term exposures and typically results from repeated occupational exposures (eg, in radiology technicians). The injuries are similar to those noted above but tend to be more pronounced. This is particularly true of vascular damage. Fibrosis and thrombosis progress to an obliterative endarteritis and its attendant ischemia.
Given the progressive nature of radiation damage, a soft-tissue ulceration may develop at any time after radiation exposure. This ulceration may be large, or it may initially manifest as a draining sinus.
Wednesday, August 6, 2008
Principles of Microsurgery
Microsurgical reconstruction is used for complex reconstructive surgery problems when other options such as primary closure, healing by secondary intention, skin grafting, local flap transfer, and distant flap transfer are not adequate. Microsurgery may not be the best solution for all reconstructive dilemmas and certainly is not the first choice in the reconstructive ladder. However, it can offer the reconstructive surgeon a wide range of possibilities for complex reconstruction. In specific cases, such as mandibular reconstruction, free tissue transfer may be the best option. The purpose of this article is to outline the principles of microsurgery, specifically the principles of surgical planning and operative technique that will optimize success.
Flaps, Classification
A flap is a unit of tissue that is transferred from one site (donor site) to another (recipient site) while maintaining its own blood supply.
Flaps come in many different shapes and forms. They range from simple advancements of skin to composites of many different types of tissue. These composites need not consist only of soft tissue. They may include skin, muscle, bone, fat, or fascia.
How does a flap differ from a graft? A flap is transferred with its blood supply intact, and a graft is a transfer of tissue without its own blood supply. Therefore, survival of the graft depends entirely on the blood supply from the recipient site.
History of flap surgery
The term flap originated in the 16th century from the Dutch word flappe, meaning something that hung broad and loose, fastened only by one side. The history of flap surgery dates as far back as 600 BC, when Sushruta Samita described nasal reconstruction using a cheek flap. The origins of forehead rhinoplasty may be traced back to approximately 1440 AD in India. Some reports suggest flap surgeries were being performed before the birth of Christ.
The surgical procedures described during the early years involved the use of pivotal flaps, which transport skin to an adjacent area while rotating the skin about its pedicle (blood supply). The French were the first to describe advancement flaps, which transfer skin from an adjacent area without rotation. Distant pedicle flaps, which transfer tissue to a remote site, also were reported in Italian literature during the Renaissance period.
Subsequent surgical flap evolution occurred in phases. During the First and Second World Wars, pedicled flaps were used extensively. The next period occurred in the 1950s and 1960s, when surgeons reported using axial pattern flaps (flaps with named blood supplies). In the 1970s, a distinction was made between axial and random flaps (unnamed blood supply) and muscle and musculocutaneous (muscle and skin) flaps. This was a breakthrough in the understanding of flap surgery that eventually led to the birth of free tissue transfer.
In the 1980s, the number of different tissue types used increased significantly with the development of fasciocutaneous (fascia and skin) flaps (which are less bulky than muscle flaps), osseous (bone) flaps, and osseocutaneous (bone and skin) flaps.
The most recent advancement in flap surgery came in the 1990s with the introduction of perforator flaps. These flaps are supplied by small vessels (previously thought too small to sustain a flap) that typically arise from a named blood supply and penetrate muscle, muscle septae, or both to supply the overlying tissue. An example of this is the deep inferior epigastric perforator (DIEP) flap, which has now become the criterion standard in breast reconstruction.
Classification of flaps
Most classification systems have been designed for the sole purpose of aiding communication with peers by being familiar with the correct vocabulary to use. However, the crucial point for any physician to remember is that communication with the patient is of foremost importance. The patient must be able to picture, with the surgeon's guidance, what the surgeon is planning.
Many different methods have been used to classify flaps. Furthermore, these classification systems are often complex and varied in principle.
To improve the reader's understanding of flap classification, the author has summarized the most commonly used classifications into 3 simplified categories: type of blood supply, type of tissue to be transferred, and location of donor site.
- Blood supply
- Like any living tissue, flaps must receive adequate blood flow to survive. A flap can maintain its blood supply in 2 main ways.
- If the blood supply is not derived from a recognized artery but, rather, comes from many little unnamed vessels, the flap is referred to as a random flap. Many local cutaneous (skin) flaps fall into this category. If the blood supply comes from a recognized artery or group of arteries, it is referred to as an axial flap. Most muscle flaps have axial blood supplies.
- Because of the complexity and variation observed in axial blood supply, a further subclassification (axial types I-V) was made by Mathes and Nahai and is readily used in plastic and reconstructive surgery literature to describe different types of muscle flaps (see Image 1).1
- The classification of flaps based on blood supply, including the Mathes and Nahai subclassification, can be summarized as follows:
- Random (no named blood vessel)
- Axial (named blood vessel) Mathes and Nahai classification
- One vascular pedicle (eg, tensor fascia lata)
- Dominant pedicle(s) and minor pedicle(s) (eg, gracilis)
- Two dominant pedicles (eg, gluteus maximus)
- Segmental vascular pedicles (eg, sartorius)
- One dominant pedicle and secondary segmental pedicles (eg, latissimus dorsi)
- Tissue to be transferred
- In general, flaps may comprise in part or in whole almost any component of the human body, as long as an adequate blood supply to the flap can be ensured once the tissue has been transferred.
- Flaps may be composed of just one type of tissue or several different types of tissue. Flaps composed of one type of tissue include skin (cutaneous), fascia, muscle, bone, and visceral (eg, colon, small intestine, omentum) flaps. Composite flaps include fasciocutaneous (eg, radial forearm flap), myocutaneous (eg, transverse rectus abdominis muscle [TRAM] flap), osseocutaneous (eg, fibula flap), tendocutaneous (eg, dorsalis pedis flap), and sensory/innervated flaps (eg, dorsalis pedis flap with deep peroneal nerve).
- Therefore, another way of classifying flaps is by describing the different types of tissue that are being used in the flap.
- Location of donor site
- Tissue may be transferred from an area adjacent to the defect. This is known as a local flap. It may be described based on its geometric design, be advanced, or both. Pivotal (geometric) flaps include rotation, transposition, and interpolation. Advancement flaps include single pedicle, bipedicle, and V-Y flaps.
- Tissue transferred from an noncontiguous anatomic site (ie, from a different part of the body) is referred to as a distant flap.
- Distant flaps may be either pedicled (transferred while still attached to their original blood supply) or free. Free flaps are physically detached from their native blood supply and then reattached to vessels at the recipient site. This anastomosis typically is performed using a microscope, thus is known as a microsurgical anastomosis.
Now that the main ways of classifying flaps have been introduced, the remaining sections of this article are devoted to the most important principles to remember before performing flap surgery. Like any surgical procedure, flap surgery is not devoid of risk. Complications such as complete flap loss can be catastrophic. Considering the following basic principles before any flap surgery serves patients well by optimizing outcome and decreasing operative morbidity.
Facial Trauma, Frontal Sinus Fractures
Fractures of the frontal sinus pose certain treatment dilemmas to the facial trauma surgeon. Their mismanagement may lead to potentially life-threatening intracranial complications, most commonly meningitis, encephalitis, and brain abscess. Other complications include frontal osteomyelitis, frontal bone non-union, cavernous sinus thrombosis, cerebrospinal fluid (CSF) leak, mucopyocele, and meningoencephalocele (Metzinger, 2005). These injuries are currently managed by various medical specialists, including otolaryngologists/head and neck surgeons, maxillofacial surgeons, plastic surgeons, and neurosurgeons. As a result, consensus does not exist regarding the timing, indications, and treatment modality of these injuries. The series reported in the literature have relatively few subjects and, as might be expected, mostly limited follow-up periods.
In the past, roentgenograms were used for diagnosing frontal sinus fractures, although the sensitivity of plain films was well-recognized as not very high (May, 1970). Roentgenography can result in underdiagnosis and is not particularly useful in examining the severity of damage to the posterior table and the nasofrontal duct region (Harris, 1987).
The use of high-resolution, 1.5-mm axial and coronal thin-cut computed tomography (CT) scanning provides improved diagnostic power for assessing injuries to the frontal sinus and midface (Johnson, 1984; Schatz, 1984; Harris, 1987) and has become invaluable in the diagnosis of frontal sinus fractures. Involvement of the nasofrontal duct is not easily discernible with CT imaging and, as a result, decisions regarding management of the nasofrontal duct and frontal sinus are frequently made during surgical exploration. However, nasofrontal duct injury is strongly suggested when the CT scan demonstrates involvement of the base of the frontal sinus, the anterior ethmoid complex, or both (Harris, 1987). The nasofrontal duct complex should be evaluated in both the axial and coronal planes.
History of the Procedure
The progression of frontal sinus surgery stems from the first ablative procedure described by Reidel in 1898. He described total exoneration of the sinus by removing the anterior table and floor of the sinus, allowing the skin to overlay the posterior table. This technique created an obvious marked cosmetic defect. In 1904, Killian described a similar procedure, but this procedure left a 10-mm rim of supraorbital bone, improving the cosmetic result.
In 1921, Lynch described the first frontoethmoidectomy, leaving the anterior table intact but completely removing the ethmoid sinuses and the frontal sinus floor. An indwelling catheter was inserted for prolonged drainage.
In 1951, Bergara and Itoiz devised the osteoplastic flap procedure. They described exposure of the sinus by removing the anterior table, but, unlike Reidel, it was left hinged to an inferiorly based pedicle of pericranium. The flap was replaced at the end of the procedure. This technique resulted in a marked improvement in the overall aesthetic result.
In the late 1950s and 1960s, Goodale and Montgomery first described the ablative frontal sinus procedures that are the basis for current surgical obliterative management of frontal sinus fractures. They took the osteoplastic flap procedure one step further, describing methods of ablating the frontal sinus by grossly removing all sinus mucosa and packing it with autogenous fat, essentially eliminating the sinus as a functional unit.
Later work described the involvement of the nasofrontal ducts in chronic complications of frontal sinus trauma, presumably secondary to duct stenosis (May, 1970). It then became clear that simple obliteration as described by Goodale and Montgomery was insufficient to completely prevent the occurrence of late sequelae. The importance of removing any retained mucosa in the region of the nasofrontal duct was stressed (May, 1970; Levine, 1986). Failure to remove all sinus mucosa and subsequent reepithelialization of the sinus was demonstrated to result in late complications such as mucoceles and mucopyoceles.
Donald and Bernstein described the first cranialization procedure in 1978. It involved stripping the sinus of all mucosa, plugging the nasofrontal ducts, and removing the posterior table, allowing the brain to expand into the frontal sinus space; the procedure thus incorporated the previous frontal sinus space into the anterior cranial vault. This procedure is still used today, but it is usually reserved for patients with severe comminution of the posterior table.
Problem
Frontal sinus fractures can be classified into fractures of the anterior table, the posterior table, or both. Isolated fractures of the posterior table are rare. The fractures may be simple, comminuted, displaced, or nondisplaced. Displacement of anterior table fragments, especially when through the inferior and/or base half of the sinus, can cause obstruction of the nasofrontal duct (May, 1970). Displacement of the anterior table can also lead to depression of the forehead and a cosmetic deformity (see Images 1-2).
Posterior table fractures usually occur in combination with fractures of the anterior table and are frequently associated with intracranial trauma. When the posterior table is displaced more than the width of the table, the incidence of CSF leak and dural tears is high. Impinged sinus mucosa between fracture segments may lead to the formation of mucoceles (Bordley, 1973). The frequency of nasofrontal duct injury is proportional to the severity and comminution of the frontal sinus fracture. Injuries to the duct are likely when the fracture is medial to the supraorbital notch and involves the base of the frontal sinus and/or the anterior ethmoid complex (see Images 3-4). Unrecognized injury to the nasofrontal duct may lead to frontal sinus drainage and aeration obstruction and, eventually, the formation of mucoceles, mucopyoceles, meningitis, and intracranial abscess.
Frequency
Frontal sinus fractures comprise 5-12% of maxillofacial traumas (May, 1970; McGraw-Wall, 1998; Gerbino, 2000). The incidence appears to be approximately 9 cases per 100,000 adults (Wright, 1992).
Etiology
Fractures of the frontal sinus occur most commonly as a result of blunt trauma from a motor vehicle accident; the next most common cause is high-impact sports-related injury (Shockley, 1988; Wright, 1992; Gerbino, 2000; Yavuzer, 2005). Frontal sinus fractures may result from low-velocity, high-velocity, blunt, or penetrating trauma. With low-velocity impact, the anterior table may confer some protection to the posterior table and may be the only table to fracture. Conversely, high-velocity or penetrating trauma may cause severe damage to both the anterior and posterior tables, with comminution and significant displacement (Rohrich, 1992).
Pathophysiology
The force required to fracture the frontal sinus has been reported to be 800-2200 lb of force and is usually sufficient to cause significant associated injuries (Nahum, 1975).
Clinical
Patients presenting with this type of injury usually have associated craniofacial trauma, which must be treated in an appropriately triaged fashion. Patients may present in a coma 20-76% of the time, depending on the series studied (Rohrich, 1992; Wright, 1992; Yavuzer, 2005). As many as 93% of patients present with multiple associated facial fractures, skull fractures, or both (Rohrich, 1992; Wright, 1992). In one series, 20% of patients presented with CSF rhinorrhea (Yavuzer, 2005).
A fracture of the frontal sinus should be considered clinically when a gross depression or laceration is found over the supraorbital ridge, glabella, or lower forehead, as this is the most common finding on clinical examination (Harris, 1987). Lacerations should be examined gently to determine if any bony step-offs are present. As many as 59% of these patients may present with orbital trauma (Levine, 1986). Prompt ophthalmologic evaluation may be necessary. A large percentage of patients also may have associated fractures of the naso-orbito-ethmoid complex and midface, which may also suggest involvement of the nasofrontal duct. Gross CSF rhinorrhea may occur if the posterior table of the frontal sinus and the dura are involved in the injury.
Craniosynostosis Management
Most of the modern understanding of craniosynostosis is referenced from the 1851 writings of Virchow. His understanding and descriptions of irregular calvarial growth patterns were the basis of the law of Virchow. According to his observations, the abnormal cranial growth observed in persons with craniosynostosis occurs perpendicular to the involved calvarial sutures. Therefore, if a suture line is prematurely ossified, no growth is present in the direction perpendicular to that suture. The law was too simplistic in its explanation of the growth patterns of the skull; later studies demonstrated conflicting data (Moss, 1959). The presence of compensatory growth patterns in patients with craniosynostosis was described later (Delashaw, J Neurosurg, 1989; Delashaw, Neurosurg Clin N Am, 1991).
Surgical treatment for craniosynostosis was initially advocated by Lannelongue in 1890. His patients had microcephaly from craniosynostosis and were thought to be imbeciles. These patients accordingly underwent craniectomy to remove the involved suture line and to "release the brain" (Lannelongue, 1890). Soon after, in 1891, linear craniectomy was introduced. As with any new procedure, this one met with much resistance. However, the resistance to a surgical intervention was slowly put to rest with mounting evidence. Several studies indicated that craniosynostectomy was the treatment of choice for the release of fused suture lines in the skull (Faber, 1927; Dandy, 1943; Ingraham, 1948; Shillito, 1968).
Although strip craniectomy was used often, it lost much support with the advent of cranial vault reconstruction, in which the calvarial bones were excised, reshaped, and trimmed. Studies showed that, over time, cranial suture areas excised during strip craniectomy still became fused and led to an abnormal cranial contour (Venes, 1976). Strip craniectomy was easier and involved less blood loss compared with the newer cranial vault reconstruction. Strip craniectomy also did not address the frontal bossing and associated abnormalities in calvarial shape and relied on the rapid growth of the brain to correct it. Strip craniectomy was optimal only in the first few months of infancy, while surgeons could use cranial vault reconstruction throughout infancy. Consequently, strip craniectomy lost favor, and the surgical treatment has been modified to include cranial vault remodeling.
Recently, with the advent of endoscopy, attention has returned to endoscopic strip craniectomy. The endoscopic technique has only been tried over the last several years, but it offers the advantages of a shorter and safer operation, less cost, less in-hospital time, and less blood loss. The operation was shown to be a success in a study of 12 patients, all younger than 8 months (Barone, 1999). Critical to this success and a departure from the standard strip craniosynostectomy was the extensive use of a postoperative remodeling helmet. Although first introduced by Persing et al in 1986, helmet therapy has not been used as extensively as a postoperative therapeutic intervention (Persing, 1986). Following the endoscopic technique, helmets were used for several months and showed promising early results.
Craniofacial, Asian Malar and Mandibular Surgery
Aesthetics of the malar-mandibular area
Malar reduction surgery
Etiology: The etiology of this condition is unknown.
Clinical: Patients requesting zygoma reduction surgery may simply wish to have a more balanced appearance. East Asian cultures value a small face, and wide cheekbones appear to make the face bigger. In other cases, patients may attribute some misfortune in their life to the zygomatic prominence and wish it corrected for this reason. The patient with a prominent mandibular angle generally seeks aesthetic improvement. A prominent jawline creates a masculine appearance that may be undesirable. Because Asian beauty emphasizes subtlety, a prominent jawline throws off the balance of subtle midfacial features (nose, chin) by overpowering the mid face. Reducing the jawline restores the balance. When it comes to the prominent jawline, patients may have a significant muscle component, bone component, or both.Congenital Syndromes
This collection of syndromes has proved to be an exciting area of investigation for plastic surgeons and other researchers. Surgeons currently have better tools to diagnose and investigate these syndromes, and they are now better understood. Most exciting of all, more sophisticated treatment methods have evolved over the past 20 years.
Crouzon Syndrome
Crouzon syndrome was first described in 1912.
Inheritance
Inheritance is autosomal dominant with virtually complete penetrance. It is caused by multiple mutations of the fibroblast growth factor receptor 2 gene, FGFR2 (Gorry, 1995; Steinberger, 1995).
Features
Features of the skull are variable. The skull may have associated brachycephaly, trigonocephaly, or oxycephaly. These occur with premature fusion of sagittal, metopic, or coronal sutures, with the coronal sutures being the most common. In addition, combinations of these deformities may be seen (Kreiborg, 1982). See Image 1.
The orbits are shallow with resulting exorbitism, which is due to anterior positioning of the greater wing of the sphenoid. The middle cranial fossa is displaced anteriorly and inferiorly, which further shortens the orbit anteroposteriorly. The maxilla is foreshortened, causing reduction of the orbit anteroposteriorly. All these changes result in considerable reduction of orbital volume and resultant significant exorbitism. In severe cases, the lids may not close completely. The maxilla is hypoplastic in all dimensions and is retruded. This decreases the anteroposterior length of the orbital floor.
The upper dental arch is narrowed and retruded, which yields a class III malocclusion. Premature contact of the molars also may be present, resulting in an anterior open bite. This may cause the mandible to be rotated downward and backward. The chin and malars are hypoplastic.
Investigations
Examination of the eyes by an ophthalmologist is essential to assess for papilledema, which indicates elevated intracranial pressure. Another finding may be optic atrophy; fortunately, this is rare.
Radiological examination
This consists of standard radiology to produce anteroposterior, lateral, and cephalometric views. The information gained is the position of the maxilla relative to the mandible. This is class III, with the upper teeth lying behind the lower teeth when they are in occlusion. Patients show evidence of elevated intracranial pressure and have "paw marking" of the skull due to the gyri of the brain indenting and thinning the calvaria, with, in severe cases, erosion (see Image 2). The fusion of the involved sutures can be seen.
A CT scan helps confirm the findings of standard radiographs and provides information on ventricular size. Three-dimensional CT scans can be produced but yield no more information than standard scans, although suture fusion can be graphically displayed.
General assessment
Other abnormalities are sought, and the child's mental development is carefully assessed. An orthodontist should see the child and initiate treatment when indicated.
Apert Syndrome
In nearly all patients with Apert syndrome, the cause is 1 of 2 FGFR2 mutations involving amino acids (Ser252Trp, Pro253Arg). The condition is inherited in an autosomal dominant mode.
Craniosynostosis is present, characterized by brachycephaly and, frequently, turricephaly; the anterior fontanelle is enlarged (Kreiborg, 1991). The maxilla is hypoplastic with a high-arched palate, class III malocclusion with an anterior open bite, and, frequently, a cleft of the soft palate. The mid face is hypoplastic. Together with the retrusion, this causes exorbitism. Complex syndactyly of the hands and feet is present. It is symmetric, and other limb anomalies (eg, shortening) may be observed. The syndactyly may show fusion of the second and forth fingernails, which also may be seen in the toes (Green, 1982). See Image 3. Upper eyelid ptosis with an antimongoloid slant may be seen. Blindness may be present. Overall, the deformity is worse than that of Crouzon syndrome.
Pfeiffer Syndrome
This is an autosomal dominant condition caused by a single recurring mutation (Pro252Arg) of the FGFR1 gene and several mutations involving FGFR2. Patients have craniosynostosis, enlarged thumbs and great toes, and a hypoplastic mid face. The hypoplastic mid face gives the forehead an enlarged appearance. The nose is small. Exorbitism may be present, but it is never as prominent as in persons with Crouzon or Apert syndrome. The condition has been classified into 3 types. Patients with type I have the best long-term prognosis, whereas those with types II and III have neurologic compromise and die young (Cohen, 1993).
Saethre-Chotzen Syndrome
This is an autosomal dominant condition with full penetrance. It is caused by multiple mutations of FGFR2. Craniosynostosis is present, and the hairline is low. Ptosis and brachydactyly are characteristic. The forehead is retruded, giving the appearance of slight exorbitism. The maxilla may or may not be retruded.
Carpenter Syndrome
Patients with this autosomal recessive condition have craniosynostosis, syndactyly of the feet, and short hands and fingers with syndactyly of varying degrees.
Treatment of Craniosynostosis Syndromes
The age at presentation determines the treatment. If possible, provide treatment early and direct it at the cranial vault. The aim is to reduce intracranial pressure, if present, and to prevent visual problems. In addition, the patient's appearance may be improved. The anterior cranial fossa enlargement is a result of frontal lobe growth; at 11 months, the frontal lobes are almost 50% of adult size. The anterior cranial base is at 56% of its total growth at birth and, at 2 years, has achieved 70% of its total growth, probably soon after this full growth is attained. The size and position of the anterior and middle cranial fossa floors are determined by the frontal and temporal lobes. If the anteroposterior growth of the skull base is diminished, this has no affect on mandibular growth.
Early skull base suture fusion results in interference with forward facial growth; thus, release of the affected sutures should provide normal growth. This certainly is the case for the skull, but the mid face remains intruded in patients with Apert or Crouzon syndrome.
Undoubtedly, the best results are achieved in patients with isolated sagittal craniosynostosis. In the past, this was managed with a sagittal strip craniotomy. Currently, making coronal and lambdoid cuts to achieve immediate lateral expansion by hinging the cranial segments outwards is more common. Do not interfere with the lambdoid and coronal sutures.
At 9-11 months in persons with bilateral coronal craniosynostosis, as is seen in Crouzon or Apert syndrome, the frontal area and supraorbital rims are osteotomized separately and advanced to produce a degree of overcorrection with improved frontal contour (Posnick, 1992). This also requires a cut through the orbital roofs and in front of the cribriform plate anteriorly. Laterally in the temporal fossa, the supraorbital rim is advanced using tongue-and-groove techniques for stabilization, although this is now not absolutely necessary because plates and screws (metal or absorbable) are available. The frontal bone is now advanced and plated onto the newly positioned supraorbital rim (see Image 4).
Even with large advancements, scalp closure is always possible. Occasionally, this is aided by galeal scoring. Although this is a standard technique, it is modified as required by the basic anatomy. The patient is monitored using postoperative CT scans to follow the resolution of the dead space (see Images 5-6).
Distraction
Currently, the trend is to advance and fix the frontosupraorbital region and to advance the maxilla subsequently or at the same time, even at an early age, with (Chin, 1997) or without (David, 1990) a distraction apparatus. Although internal distraction devices have been used to push the maxilla forward, with fixation on the temporal area and the use of a rod to apply an anterior pushing on the lateral orbital walls, these have not been uniformly successful. This is mainly because of design faults.
The rigid external distraction device, which is secured by skull fixation, with an anterior pulling force being applied to the maxilla, is more mechanically sound and works well (Figueroa, 1999). It is expensive, the fixation can penetrate the cranium (should the patient fall, striking the side of the head), and the device can become displaced (Rieger, 2001).
Despite this, good forward maxillary movement is obtained in a relatively controlled fashion (see Image 7). The children do not complain about wearing this device. It can be used for persons with Crouzon or Apert syndrome or other conditions that require an osteotomy and forward pull. Whether this is an advantage over the older, well-established, and safe method of advancement osteotomy, stabilization, and bone grafting in one stage remains unproved. In older patients, the latter method probably remains the technique of choice.
Empyema and Bronchopleural Fistula
Empyema thoracis has many causes, but the most common causes in order of magnitude are pulmonary infection and previous surgical resection of lung. These two etiologies represent 70-80% of empyemas in most series. Those patients with empyema treated by plastic surgeons commonly have undergone previous surgical resection and have developed a bronchopleural fistula.
History of the Procedure
Early treatment of empyema involved open drainage. In 1935, Eloesser described a skin flap procedure that creates a permanent fistula to drain the pleural space; however, his experience was not apparently reported until 1969. In 1938, Carter described the use of muscle flaps in the closure of chronic empyema cavities. His rationale was based on the acceptance of muscle flap coverage of osteomyelitic defects.
Problem
Empyema thoracis is a collection of pus within the pleural space. Since the thoracic cavity is rigid, obliterating dead space in the thoracic cavity is more difficult than in soft tissue. For example, fluid naturally fills any vacancies made by abscesses or lung resection. If the fluid becomes seeded with bacteria, either hematogenously or through direct contact, it initiates an inflammatory response that eventually leads to organization of a fibrous peel and trapped lung parenchyma. Bronchopleural fistulas occur following pulmonary resections because of failure of the bronchial stump to heal and may lead to empyema when not quickly recognized and treated. In addition, bronchopleural fistulas put the contralateral lung at risk of being seeded with bacteria from the infected hemithorax.
Frequency
Empyema most commonly occurs following pulmonary infection and in approximately 1-3% of lung abscesses. Streptococcus species are responsible for most empyema secondary to community-acquired pneumonia. However, hospital-acquired cases have a broader bacteriology, including methicillin-resistant Staphylococcus aureus, Pseudomonas species, and Escherichia coli. The second most common cause is previous surgical procedures, including surgery of the lungs, esophagus, or mediastinum. Empyema occurs in 2-12% of patients following these procedures.
Etiology
Bronchopleural fistulas result following failure of the bronchial stump to heal. This failure to heal may be from improper initial closure, inadequate blood supply, infection at the bronchial stump, or residual malignant tumor at the bronchial stump.
Pathophysiology
The American Thoracic Society has classified empyema into 3 phases based on the natural history of the disease. The first phase is the exudative phase and involves the release of sterile pleural fluid into the pleural space in response to inflammation of the pleura. At this stage, the pleura and related lung are mobile.
The second phase has been termed the fibrinopurulent or transitional phase. During this stage, the pleural fluid becomes more turbid and fibrin develops on the pleural surfaces. At this time, pleural fluid becomes viscous. The fibrin peel loculates the fluid collection and gradually limits expansion of the underlying lung.
The final phase is the organizing or chronic phase, during which time the peel begins to organize with ingrowth of capillaries and fibroblasts. The lung has now become completely trapped within the peel and cannot expand to fill the empyema cavity.
Clinical
Clinical presentation depends on the underlying cause of the empyema. Most patients report dyspnea with little exertion, and they usually have a low-grade fever early in the course. Later on, patients may experience pleuritic chest pain and a feeling of heaviness on the affected side of the chest. They may also experience purulent sputum. On physical examination, breath sounds are decreased on the involved side of the chest. In addition, the affected hemithorax may be less mobile than the unaffected hemithorax. Chest radiographs are the appropriate first study and usually show opacifications and may show air-fluid levels. CT scans are invaluable to elucidate loculation and to direct appropriate drainage of the area.
Chest Reconstruction, Sternal Dehiscence
n thoracic and trunk reconstruction, plastic surgery plays a major role in addressing wound healing problems, complex defects, and cancer reconstruction. The introduction of the midline sternotomy incision allowed access to mediastinal structures and greatly propelled the field of thoracic surgery. The ability to gain access to the mediastinal organs through this approach allows the safe and effective treatment of cardiothoracic disease today.
History of the Procedure
Early use of the midline sternotomy was fraught with high complication rates. Sternal wound infection occurred in as many as 5% of patients, leading to sternal wound dehiscence, with reported incidence of mediastinitis in 0.4-6.9% of patients. These complications often led to significant morbidity, with reported mortality rates of more than of 50%. Sternal dehiscence initially was treated conservatively with open drainage and debridement with packing. Graft exposure, desiccation of wound margins, osteomyelitis, and, ultimately, sudden death, were grave consequences. This led to closed management with catheter-antibiotic irrigation; however, the mortality rate remained approximately 20%.
The management of infected sternal wounds changed with the principles of wide debridement and muscle and musculocutaneous flap transposition. In 1976, Lee introduced the greater omentum flap. Jurkiewicz et al then demonstrated the effectiveness of pedicled muscle flaps for management of sternal dehiscence and infection. The use of vascularized regional tissue allowed for greater blood flow, obliteration of dead space, and faster healing time because of quicker resolution of infection. Today, the management of sternal dehiscence and infection involves wide debridement of devitalized infected soft tissue and bone, culture-specific antibiotics, and flap closure (eg, muscle, musculocutaneous, omentum) to achieve wound healing. Thus, the mortality rate from sternal wound dehiscence dropped to less than 10%.
Etiology
Factors associated with sternal wound dehiscence
Numerous studies were performed to identify causative factors of sternal wound dehiscence and subsequent infection. Factors identified include hypertension, smoking, diabetes, obesity, the use of an intra-aortic balloon pump, and the use of bilateral internal mammary arteries (IMAs). Females are at greater risk than males. Prolonged postoperative ventilatory support is also implicated.
Clinical
In one study, factors associated with mortality included septicemia, perioperative myocardial infarction, and an intra-aortic balloon pump. Strict aseptic technique; attention to hemostasis; and precise, motionless sternal approximation are advocated to prevent mediastinitis. In the clinical evaluation of suspected mediastinitis or sternal dehiscence, careful examination of the patient is warranted. Findings of erythema, fever, increased leukocyte count, and sternal instability are important. If clinical deterioration of the patient or further signs of breakdown are observed (ie, increased erythema, drainage, separation of incision), obtain wound cultures, administer appropriate antibiotics, and perform swift aggressive debridement followed by early flap coverage. This combination can reduce the incidence of mortality, decrease hospital stay, rapidly propel the patient's recovery from thoracic surgery, and avert the complications of mediastinitis.
Chest Reconstruction, Chest Wall Reconstruction
History of the Procedure
The history of chest wall reconstruction illustrates the challenges associated with this type of repair. In 1778, Aimar resected the first osteosarcoma of the ribs. In 1820, Cittadini reported a case of bony chest wall tumor resection. Parham, in 1899, was the first in the United States to report resection of a bony chest wall tumor involving 3 ribs. This apparently caused a pneumothorax, which was controlled with soft tissue coverage. In the early 1900s, Fell and O'Dwyer described intubation techniques and positive-pressure ventilation.
In 1906, Tansini used the latissimus dorsi myocutaneous flap, apparently for the first time, for coverage of radical mastectomy defects. Hutchins and Campbell shared this approach. Graham and Singer were the first to successfully perform a pneumonectomy in the early 1930s. In the 1940s, Watson and James used the fascia lata for closure of skeletal wound defects. Bisgard and Swenson described the use of ribs for closure of sternectomies.
Pickrell offered techniques in chest wall resection for breast cancer, and Maier described his use of cutaneous flaps for patients with breast cancer postresection. The 1950s and 1960s included refinement of the reconstructive techniques and the implementation of multistaged procedures. Other pioneers of mention include Arnold and Pairolero, whose studies concluded that chest wall reconstruction is safe, durable, and associated with long-term survival. For the past 25 years, chest wall reconstruction has undergone a vast growth in technique and alternatives. Flaps often used for this task are the latissimus dorsi, pectoralis major, serratus anterior, rectus abdominis, external oblique, and omentum.
The congenital defect of the thorax, Poland syndrome, was described by Sir Alfred Poland in 1841. He noted restricted musculature on one side of the thorax on a single autopsy. In his report entitled "Deficiency of the pectoralis muscle," he described absence of the sternocostal portion of the pectoralis major, an absent pectoralis minor, and a severely hypoplastic serratus anterior and external oblique. de Haan associated the defects of Poland syndrome to the overlooked concomitant deformities of the ipsilateral upper extremity and hand.
Etiology
One of the most common acquired chest wall deformities is sequela from infection. This may be the result of mediastinitis, trauma, or empyema. The resulting defects, from debridement of the chest wall or the pleural space and its contents, may require fill procedures with flaps of thoracic or abdominal origin, sterilization procedures, or collapse procedures as in thoracoplasty. Tumor radiation injury promoting scar and nonfunctional tissue also may require debridement and reconstructive measures. Resection of large chest wall, pulmonary, or mediastinal tumors, as well as defects created by trauma, may merit chest wall reconstruction.
The etiology of Poland syndrome, a congenital defect of the chest wall, is unclear, yet the current theory describes hypoplasia of the ipsilateral subclavian artery in utero. The subclavian artery supply disruption sequence (SASDS) described by Parker et al illustrates the kinking of the upper extremity artery as the ribs grow forward and medially. The reduction in lumen diameter and thus flow impedes distal growth, which supports the theory that more proximal blocked flow results in more severe deformity. The incidence of Poland syndrome is 1 in 30,000. The right side in Poland syndrome is affected twice as often as the left and it is considered to be autosomal dominant with low penetrance.
Möbius syndrome involves the anomalies observed in Poland syndrome in addition to bilateral facial paralysis and the inability to abduct the eyes. Möbius syndrome is observed in 1 individual per 500,000.
The etiologies of pectus excavatum and pectus carinatum are unknown. Pectus excavatum is the most common congenital anomaly of the chest (90%). The male-to-female ratio is 3:1.
Pathophysiology
The muscles of inspiration, an active action, involve primarily the diaphragm, which contracts inferiorly and creates a negative intrapleural pressure, thus inducing inhalation. Secondary muscles involved in inspiration are termed accessory muscles and are the sternocleidomastoids, which aid in raising the sternum superiorly and outward; the scalene muscles, which elevate the upper ribs; and the external intercostal muscles, which elevate all the ribs.
Expiration is a passive process. The intrinsic elasticity of the lung and musculature promotes exhalation. The muscles mentioned above relax and initiate the expiratory phase of breathing. Pulmonary function tests that measure forced expiratory volume in 1 second (FEV-1), tidal volume, and the ratio of FEV-1 to forced vital capacity ratio also are beneficial, yet these values are not critical in the face of mandatory surgical intervention. Lung disease takes on two broad categories, obstructive and restrictive. With obstructive disease, expiration is impeded by proximal obstruction of the bronchioles and bronchi, causing air trapping, increased functional residual capacity and residual volume, and decreased FEV-1 and vital capacity.
Restrictive lung disease is an interstitial process that causes lung tissue to be less compliant, thus reducing the ability of the lung to expand. This promotes reduced lung volumes. Flail chest refers to a segment of chest wall, usually 5 cm in diameter, which loses continuity with the surrounding chest wall, resulting in a paradoxic respiratory pattern and inefficient ventilation. Adequate fixation of this segment is necessary to correct this phenomenon and restore proper respiratory physiology and ventilation.
The size of the defect above which bony stabilization is required is not clear. Two-rib segmental loss may be repaired with soft tissue reconstruction. While Dingman cautions that a 4-rib loss results in flail, Arnold argues that complete sternectomy or resection of 4-6 ribs at the cartilage level does not result in flail or respiratory instability. McCormack and Picciocchi et al agree that defects less than 5 cm in diameter or resection of 3 ribs or fewer do not merit skeletal stabilization.
Cold Injuries
Body temperature may fall as a result of heat loss by radiation, evaporation, conduction, and convection.2 Radiation causes 55-65% of the body's heat loss. Evaporation occurs via the skin and airway and accounts for 30% of the heat loss. Normally, in a dry environment, only 15% of the body's heat loss results from conduction. However, the thermal conductivity of water is approximately 30 times that of air, so the body loses heat rapidly when immersed in water or covered in wet clothing, leading to a rapid decline in body temperature. Convection accounts for a minor amount of heat loss, but it becomes more significant in a windy environment. The amount of heat dissipated by any of these mechanisms is proportional to the temperature difference between the body and environment.
Opposing the loss of body heat are the mechanisms of heat conservation and gain. In general, a thermostat in the preoptic region of the hypothalamus controls these mechanisms. This human thermostat is set to a precise reference temperature, usually very close to 37°C (98.6°F). It responds to thermoregulatory mechanisms, the temperature of blood, and temperature receptors deep within the body and in the skin.
When the preoptic area of the hypothalamus is stimulated, various heat conservation and production mechanisms become activated. When the sympathetic nerves are excited, they cause the blood vessels in the skin to markedly constrict. The flow of warm blood from the core of the skin is depressed, thereby reducing the transfer of heat to the body surface. This reduction of blood flow in the skin is the prime physiologic regulator of heat loss from the body. The temperature of the skin decreases to approach the temperature of surrounding air, which lowers the temperature gradient and further decreases heat loss.
Stimulation of the sympathetic nerves also causes secretion of epinephrine and norepinephrine by the adrenal medullae. These hormones increase the metabolic rate of all cells, thereby enhancing heat production. Impulses from the preoptic hypothalamus also activate the primary motor center for shivering, which, in turn, increases the tone of muscles. The resulting enhancement of muscle metabolism can increase heat production by as much as 500%.
Causes
Hypothermia or systemic cold injury is a clinical condition in which the core body temperature has decreased to 35°C (95°F) or less. The causes of hypothermia are either primary or secondary. Primary, or accidental, hypothermia occurs in healthy individuals inadequately clothed and exposed to severe cooling.3 Accidental hypothermia can be divided into immersion and nonimmersion cold exposure. The high thermal conductivity of water leads to the rapid development of immersion hypothermia. Although the rate of heat loss is determined by water temperature, immersion in any water less than 16°C (60.8°F) may lead to hypothermia within minutes. (Click here to complete a Medscape CME activity on mild hypothermia therapy.)
When individuals are buried in the snow of an avalanche, they must be extricated from the scene of the avalanche accident as soon as possible.4 In fact, rapid extrication is the most important determinant of positive outcome in snow avalanche victims. To facilitate the rapid localization of avalanche victims, avalanche transceivers are widely used during off-piste and back country activities.
Hohlrieder et al conducted a retrospective study to analyze the influence of transceivers on the mortality of avalanche victims.4 In the 194 accidents in Austria between 1994-2003, 278 victims were totally buried. Avalanche transceivers were used by 156 victims (56%), and transceiver use was associated with a significant reduction in the median burial time, which decreased from 102 minutes to 20 minutes (P < .001). Transceiver use was also associated with a significant reduction in mortality, which decreased from 68.0% to 53.8%. This reduction reflects a decrease in mortality during back country activities that involved ski tourists in free alpine areas. Transceivers did not significantly reduce mortality when they were used in off-piste activities beside or near organized ski slopes.
Even if a person is using a transceiver, mortality is significantly higher if burial depth exceeds 1.5 m. Despite a significant reduction in mortality, mortality still exceeds 50% even with transceivers. Consequently, even with the use of emergency equipment and life transceivers, avoiding avalanches is critically important. The authors conclude that the fairly modest influence of the use of transceivers on survival probability may also be due to the high efficiency of the mountain rescue service in the Austrian Alps.
In secondary hypothermia, another illness predisposes the individual to accidental hypothermia. The mechanism of secondary hypothermia appears to be an acute failure of thermoregulation; shivering does not usually occur in these patients. In many reports, alcohol seems to be a predominant cause of cutaneous vasodilation, loss of shivering, hypothalamic dysfunction, and lack of concern regarding the environment.5 Other factors that predispose an individual to acute hypothermia include the following:
- Endocrine diseases (eg, hypothyroidism, pituitary insufficiency, Addison disease, diabetes mellitus6)
- Cardiovascular diseases (eg, myocardial infarction,7 congestive heart failure, vascular insufficiency)
- Neurologic diseases (eg, cerebrovascular accident, head injury, tumor, spinal cord injury, Alzheimer disease8)
- Drugs (eg, phenothiazines, barbiturates, antidepressants)
- Pancreatitis
- Cirrhosis
- Hypoglycemia
For more information on some of the conditions that predispose individuals to acute hypothermia, visit the following Medscape Resource Centers: Hypothyroidism, Diabetic Microvascular Complications, Heart Failure, and Trauma.
Clinical presentation
Hypothermia affects multiple organs.9 Initially, the metabolic rate increases, with tachycardia, tachypnea, increased muscle tone, and peripheral vascular resistance to generate maximal shivering. With continued hypothermia, the metabolism progressively declines, with bradycardia and hypoventilation and subsequent carbon dioxide retention. The heart rate drops to half its normal rate at 28°C (82.4°F), and ventricular contractility decreases. The risk of ventricular fibrillation increases at temperatures below 28°C (82.4°F). Cerebral metabolism is decreased 6-7% per 1°C drop in temperature, which results in a declining level of consciousness. Autoregulation of cerebral blood flow is impaired at temperatures below 25°C (77°F). The shivering mechanism of thermoregulation stops at 31°C (87.8°F).
The symptoms of hypothermia vary depending on the severity of the cold injury. In mild hypothermia, clinical symptoms are often vague and include dizziness, fatigue, joint stiffness, nausea, and pruritus. The skin is pale and cool as a result of peripheral vasoconstriction. The patient may exhibit lethargy, flat affect, impaired judgment, and mild confusion progressing to motor incoordination, ataxia, and slurred speech.
In severe hypothermia, mental status is further impaired, leading to hallucinations, stupor, and even coma. Atrial and ventricular arrhythmias are common with moderate hypothermia. The Osborn (J) point, an upward deflection at the junction of the QRS complex and the ST segment, can usually be seen on the ECG. The patient may appear clinically dead, with nonpalpable peripheral pulses, fixed and dilated pupils, loss of ocular reflexes, and stiff extensor posturing. Cardiac standstill usually occurs at 20°C (68°F), but one report described a survivor whose temperature was 15°C (60.8°F).
Diagnosis
The diagnosis of hypothermia is easy if the patient is a mountaineer who is stranded in cold weather.10, 11 However, it may be more difficult in an elderly patient who has been exposed to a cold external environment. In either case, the rectal temperature should be checked with a low-reading thermometer. The diagnosis of accidental hypothermia has proved elusive, largely because clinical thermometers do not record temperatures below 35°C (95°F). The only inexpensive low-reading thermometer is the Zeal (Zeal Group Ltd; London). Electronic thermometers with digital readouts and remote electric probes are made by several companies. Rectal temperature measurements are influenced by lower body temperature and probe placement. An inaccurate reading may result if the rectal probe was inserted in cold feces or to a depth of less than 15 cm.
Other methods of determining core body temperature include infrared tympanic thermometers, esophageal probes in intubated patients, and bladder thermistors embedded in a urinary catheter. The tympanic probe accurately measures hypothalamic temperature and most rapidly changes to reflect variations in core body temperature. On the basis of temperature measurements, the arbitrary classification of the level of hypothermia is mild (<34°c>
Burns, Rehabilitation and Reconstruction
To attain the objective of optimal long-term function, rehabilitation efforts must commence from the outset of burn care. Physical and occupational therapists play an essential role in the acute management of all burn patients, even those who are critically ill and those with large injuries undergoing resuscitation. If a body part is left immobile for a protracted period, capsular contraction and shortening of tendon and muscle groups that cross the joints occur. It is amazing how rapidly this process can occur (see Image 1).
Ranging and antideformity positioning
Passive ranging and antideformity positioning in the critically ill patient can prevent this. This is best done twice daily, with the therapist taking all joints through a full range of motion. The therapist must be sensitive to the patient's wounds, the status of extremity perfusion, the state of pain and anxiety, and the security of the patient's airway and vascular access devices. It is often useful to medicate patients before therapy sessions to increase their efficacy and decrease their discomfort. These procedures are important but cannot be effectively or humanely performed if they are associated with undue pain and anxiety. Ranging often can be timed to coincide with dressing changes and wound cleansing, minimizing the need for medication.
It is, of course, important that the therapist be aware of the airway and vascular access devices associated with care of the critically ill burn patient. Morbidity and mortality are associated with unexpected loss of these devices. Performing these procedures in coordination with the intensive care unit staff, with full knowledge of the location and function of endotracheal tubes, nasogastric tubes, central venous catheters, arterial catheters, and other monitoring devices, can minimize the risk of their loss. Routine in-service training of therapists facilitates adherence to necessary precautions. The 3 principal priorities for the burn therapist in the acute setting are (1) ranging, (2) splinting and antideformity positioning, and (3) establishing initial contact with the patient and family.
Preventing deformities
Properly performed antideformity positioning minimizes shortening of tendons, collateral ligaments, and joint capsules and reduces extremity and facial edema. Although splints are used less frequently than years ago, several predictable contractures occur in burn patients that can be prevented by a properly performed splinting program. These contractures generally are associated with the flexed position of comfort, except in the hands.
Flexion deformities of the neck can be minimized with thermoplastic neck splints, conformers, and split mattresses. In critically ill patients, positioning the neck in slight extension is often all that can be done. It is also important not to allow ventilator tubing to pull the head such that a contracture develops. If proper care is not taken, a rotary contracture can develop, generally with the patient turned toward the ventilator (see Image 2).
Preventing contractures
Axillary adduction contractures can be prevented by positioning the shoulders widely abducted with axillary splints, padded hanging troughs of thermoplastic material, or a variety of support devices mounted to the bed. Elbow flexion contractures are minimized by statically splinting the elbow in extension. These splints can be alternated with flexion splints to facilitate retention of full range of motion. Flexion contractures of the hips and knees are particularly common in young children but can be prevented by careful ranging and positioning. It is important to prevent these even in infants, as these contractures can interfere with subsequent ambulation. Prone positioning, although poorly tolerated by some, can assist in minimizing hip flexion contractures, and knee immobilizers can minimize knee flexion contractures.
The equinus deformity, denoting an extended ankle deformity, is a serious problem that can occur even if the ankles are not burned during protracted periods of bed rest with the ankle in extension. The ankle flexors will shorten and, even in the absence of an overlying burn, disabling contractures can result. However, they can be prevented with static positioning of the ankles in neutral and twice daily ranging. Splints designed for this purpose can cause pressure injury over the metatarsal heads or calcaneus if improperly designed.
These injuries can be prevented using local padding to distribute pressure away from the metatarsal heads and by extending the footplate of the splint beyond the heel and cutting out the area around the calcaneus.
At least twice daily inspection of all splints for evidence of poor fit or pressure injury is important. Improperly used splints can cause injury. Regular splint examination and inservicing of the nursing staff minimizes splint-related skin injury. Positioning burned extremities just above the level of the heart reduces edema and is another important aspect of antideformity positioning.
Burns, Lightning Injuries
Lightning's power has been a subject of awe since primitive times. Ancient Greeks saw it as an expression of the wrath of Zeus. Since lightning is caused by common meteorological conditions, anyone is a potential victim. Lightning strikes the earth more than 100 times each second and 8 million times per day. Worldwide, approximately 50,000 thunderstorms occur per day that may result in forest fires and injury to animals and people.
The National Weather Service estimates that 100,000 thunderstorms occur in the
In the
Lightning injury is the second most common cause of weather-related death in the
Thunderstorms and lightning are most common from June through September. Lightning strikes usually occur in the afternoon and evening, coinciding with times when people are active and outdoors. Hikers, campers, golfers, and other outdoor sports enthusiasts most often sustain lightning injuries. Lightning injuries are more common in rural or exposed environments than in the city, where high buildings have metal frames and lightning-protection devices. Most lightning injuries occur in areas with the greatest number of thunderstorms, such as the South;
The most important characteristic features of lightning injuries are multisystem involvement and widely variable severity. This article discusses the physics of lightning and the pathophysiology and treatment of lightning injuries.6 Because persons struck by lightning have a better chance of survival than persons who experience cardiopulmonary arrest from other causes, resuscitation for persons struck by lightning must be instituted immediately, followed by a comprehensive treatment program of the other systemic manifestations.7 (Click here to complete a Medscape CME activity on CPR.)
Burns, Electrical
Electricity is the flow of electrons from atom to atom.3, 4 Movement of electrons is comparable to the way water is passed along in a bucket brigade. Electrons, which comprise the current, are passed along from atom to atom. Amperage is the term used for the rate of flow of electrons. Every time 6.242 x 1015 electrons pass a given point in 1 second, 1 ampere of current has passed. The current is what can kill or hurt a victim of an electric injury. One ampere is roughly equivalent to the amount of current flowing through a lighted 100-watt light bulb.
In most materials, a number of electrons are free to move about at random until a driving force termed voltage propels them to move in one direction. A large voltage exerts a greater force, which moves more electrons through the wire at a given rate of time. Electric voltage of 380 volts or less is considered low voltage and above 380 volts, high voltage. High voltage is generated at the power plant and is transformed down to approximately 120 volts for most wall outlets in homes.
Resistance
Resistance of the human body has been likened to that of a leather bag filled with an electrolyte fluid, with high resistance on the outside and lower inside.5 Skin resistance also varies depending on moisture content, thickness, and cleanliness. Resistance offered by the callused palm may reach 1,000,000 ohms/cm2, while the average resistance of dry normal skin is 5000 ohms/cm2. This resistance may decrease to 1000 ohms/cm2 if hands are wet. Skin resistance is encountered primarily in the stratum corneum that serves as an insulator for the body. The voltage gradient in skin cannot be increased indefinitely and breaks down at low voltages. Exposure of the skin to 50 volts for 6-7 seconds results in blisters that have a considerably diminished resistance.
The dermis offers low resistance, as do almost all internal tissues except bone, which is a poor conductor of electricity. Other factors that affect the flow of electrons are the nature and size of the substance through which it passes. If the atomic structure of the material is such that the force of attraction between its nucleus and outer electrons is small, little force is required to cause electron loss. These substances (eg, copper, silver) in which electrons are loosely bound are termed conductors, because they readily permit the flow of electrons. Materials such as porcelain and glass are composed of atoms that have powerful bonds between their nuclei and the outer electrons. These materials are termed insulators because electron flow is restricted.
Resistance is a measure of how difficult it is for electrons to pass through a material and is expressed in a unit of measurement termed an ohm. The resistance offered to the flow of electricity by any material is directly proportional to its length and inversely proportional to its cross-sectional area. Electricity is transmitted by a high-voltage system, because it allows the same amount of energy to be carried at lower current, which reduces electrical loss through leakage and heating. The relationship between current flow (amperage), pressure (voltage), and resistance is described in Ohm's law, which states that the amount of current flowing through a conductor is directly proportional to voltage and inversely related to resistance.
Current (I) = Voltage (E)/Resistance (R)
Electrons set in motion by the current force (voltage) may collide with each other and generate heat. The amount of heat developed by a conductor varies directly with its resistance. Power (watts) lost as a result of the current's passage through a material provides a measure of the amount of heat generated and can be determined by Joule's law.
Power (P) = Voltage (E) x Current (I)
Because E = I x R (resistance), the above equation becomes P = I(squared) R. Consequently, the heat produced is proportional to the resistance and the square of the current. Commercial electric currents usually are generated with a cyclic reversal of the direction of electric pressure (voltage). Pressure in the line first pushes and then pulls electrons, resulting in alternating current. Frequency of current in hertz (Hz) or cycles per second is the number of complete cycles of positive and negative pressure in 1 second. The usual wall outlet (120 volts) provides a current with 120 reversals of the direction of flow occurring each second and is termed 60-cycle current. Frequency of alternating current can be increased to a range of millions of cycles per second. In direct current, electron travel is always in the same direction.
Alternating current
Alternating current has almost entirely superseded direct current, since it is cheaper and can be transformed easily into any required voltage. Most machines in industry and appliances in the home use alternating currents; therefore, workers and consumers are mainly at risk from this current. Direct current usage is primarily restricted to the chemical and metallurgical industries, ships, streetcar systems, and some underground train systems.6, 7
Electric arc
Contact with high-voltage current may be associated with an arc or light flash.8 An electric arc is formed between two bodies of sufficiently different potential (high-voltage power source and the body, which is grounded). The arc has an intense, pale-violet light and consists of ionized particles that are driven by the voltage pressure between the two bodies and are present in the space between them. Temperature of the ionized particles and immediately surrounding gases of the arc can be as high as 4000°C (7232°F) and can melt bone and volatilize metal. As a general guide, arcing amounts to several centimeters for each 10,000 volts. Burns occur where portions of the arc strike the patient. The electric arc remains the cause of most high-voltage electrical burn injuries. Because of its high frequency, the electric arc has become the basis for many standard safety precautions.
Effects of electricity on the body
Effects of electricity on the body are determined by 7 factors: (1) type of current, (2) amount of current, (3) pathway of current, (4) duration of contact, (5) area of contact, (6) resistance of the body, and (7) voltage.9 Low-voltage electric currents that pass through the body have well-defined physiologic effects that are usually reversible. For a 1-second contact time, a current of 1 milliampere (mA) is the threshold of perception, a current of 10-15 mA causes sustained muscular contraction, a current of 50-100 mA results in respiratory paralysis and ventricular fibrillation, and a current of more than 1000 mA leads to sustained myocardial contractions.
Humans are sensitive to very small electric currents because of their highly developed nervous system. The tongue is the most sensitive part of the body. Using pure direct current and 60-cycle alternating current, the first sensations are those of taste, which are detected at 45 microamperes. When subjected to 60-cycle alternating current, the threshold of perception in the hands of men and women, which is usually a tingling sensation, is approximately 1.1 mA. Using pure direct current applied to hands, the first sensations are those of warmth in contrast to tingling, detected at 5.2 mA.
Skin offers greater resistance to direct current than alternating current, thus 3-4 times more direct current is required to produce the same biologic effect elicited by alternating current. With increasing alternating current, sensations of tingling give way to contractions of muscles. The magnitude of the muscular contractions enhances as the current is increased. Finally, a level of alternating current is reached for which the subject cannot release the grasp of the conductor. The maximum current a person can tolerate when holding a conductor in one hand and still let go of the conductor using the muscles directly stimulated by the current is termed the "let-go" current. This tetanizing effect on voluntary muscles is most pronounced in the frequency range of 15-150 Hz.
Such strong muscular reactions may cause fractures and/or dislocations. Numerous reports of bilateral scapular fractures and shoulder dislocations and fractures in electric accidents attest to this occurrence. As the frequency increases above 150 Hz, the potential for this sustained contraction is lessened. At frequencies from 0.5-1 megacycle, these high-frequency currents do not elicit sustained contractions of the skeletal muscles. For 60-cycle alternating current, the let-go threshold for men and women is 15.87 mA and 10.5 mA, respectively. The lower value for women may result from their generally somewhat poorer muscular development compared to men.
Electrical accidents involving power frequency (50-60 Hz) and a relatively low voltage (150 V/cm) occasionally can result in massive trauma to the victim. Skeletal muscle and peripheral nerve tissue are especially susceptible to injury. Historically, Joule heating, or heating by electrical current, was viewed as the only mechanism of tissue damage in electrical trauma. Yet in some instances, Joule heating does not adequately describe the pattern of injury observed distant to the sites of contact with the electrical source. These victims exhibit minimal external signs of thermal damage to the skin, while demonstrating extensive muscle and nerve injury.
Recently, electroporation of skeletal muscle and nerve cells was suggested as an additional mechanism of injury in electrical burns. This mechanism is different from Joule heating, even though it is influenced by temperature. It is the enlargement of cellular-membrane molecular-scale defects that results when electrical forces drive polar water molecules into such defects. Experimental studies have documented that electroporation effects can mediate significant skeletal muscle necrosis without visible thermal changes.
High-voltage accidents
The national electric code defines high-voltage exposure as greater than 600 volts. In the medical literature, high-voltage exposure is judged as greater than 1,000 volts. In high-voltage accidents, the victim usually does not continue to grasp the conductor. Often, he or she is thrown away from the electric circuit, which leads to traumatic injuries (eg, fracture, brain hemorrhage). The infrequency with which sustained muscular contractions occur with high-voltage injury apparently occurs because the circuit is completed by arcing before the victim touches the contact. Currents that cause subjects to "freeze" to the circuit despite their struggle to be free are frightening, painful, and hard to endure, even for a short time.
Turning off power source
Consequently, a witness of the accident must turn off the power source as soon as possible. If this is not possible, the victim must be disengaged from the electric current. Wearing lineman's gloves, trained electricians must separate the victim from the circuit by a specially insulated pole. Looping a polydacron rope around the injured patient is another method of pulling him or her from the electric power source. Ideally, the first responder should stand on a dry surface during the rescue.
Muscular contractions
Tests using gradually increasing amounts of direct current produce sensations of internal heating rather than severe muscular contractions; however, sudden changes in the magnitude of direct current produce powerful muscular contractions. At the instant of interruption of the direct current, the subject occasionally falls back a considerable distance; the impact of the fall may cause a fracture. As the alternating current strength increases above 20 mA, a sustained contraction of muscles of respiration of the chest occurs.
Normal respiration returns after the current has been turned off, provided that the duration of current flow is less than 4 minutes. If sustained contractions last longer than this time interval, death from asphyxiation occurs, unless the current is stopped and mouth-to-mouth ventilation on the breathless patient is started. The pathway of current flow, involved in tetanic contractions of the muscles of respiration, is usually arm to arm or arm to leg and does not pass through the respiratory center located in the medulla of the brainstem. This center is injured in executions in the electric chair, leading to permanent respiratory arrest.
Treatment at the scene
When current flow increases above 30-40 mA, ventricular fibrillation may be induced. Numerous factors can influence the magnitude of electric current required to produce ventricular fibrillation. found to be of primary importance are duration of current flow and body weight. The threshold for ventricular fibrillation is inversely proportional to the square root of the shock duration and directly proportional to body weight.
When the heart is exposed to currents of increasing strength, its susceptibility to fibrillation first increases and then decreases with even stronger currents. At relatively high currents (1-5 amps), the likelihood of ventricular fibrillation is negligible with the heart in sustained contraction. If this high current is terminated soon after electric shock, the heart reverts to normal sinus rhythm. In cardiac defibrillation, these same high currents are applied to the chest to depolarize the entire heart.
If disconnecting the victim from the electric circuit does not restore pulses, the first responder must start cardiopulmonary resuscitation to restore breathing and circulation. (Click to complete a Medscape CME activity on minimally interrupted cardiac resuscitation.) Ideally, when they arrive at the scene of the accident, paramedics will continue this resuscitation. Field intervention should include advanced life support treatments delivered under the direction of a physician at the hospital base station using telemetered communication. Telemetered monitoring of these patients is recommended throughout transport to the advanced life support hospital facility.
These life-threatening consequences of low-voltage electric burns usually occur without any lesions of the skin at entrance and exit points of the current. An absence of local lesions indicates that the surface area of contact (current density) is large and that the heat is insufficient to produce a thermal injury; however, the smaller the surface area of the contact, the greater the density of the current and the more energy is transformed into heat that can cause local burn injury.
Burns, Chemical
Chemical injuries are commonly encountered following exposure to acids and alkali, including hydrofluoric acid (HF), formic acid, anhydrous ammonia, cement, and phenol. Other specific chemical agents that cause chemical burns include white phosphorus, elemental metals, nitrates, hydrocarbons, and tar.
Since World War II, the number of chemicals developed, produced, and used in the United States has increased dramatically. More than 65,000 chemicals are available on the market, and an estimated 60,000 new chemicals are produced each year. Unfortunately, the potential deleterious effects on human health of many of these chemicals are unknown. The Superfund Amendments and Reauthorization Act (SARA) contains extensive provisions for emergency planning and the rights of communities to be informed of toxic chemical releases.1
In addition to individualized state health departments, the following 5 national sources provide information regarding death and injuries caused by chemical releases: National Response Center (NRC), Department of Transportation (DOT), Hazardous Materials Information System (HMIS), Acute Hazardous Events (AHE) Database, and American Poison Control Centers Association.2
Health departments from 5 states (Colorado, Iowa, Michigan, New Hampshire, and Wisconsin) evaluated 3,125 emergency chemical-release events involving 4,034 hazardous substances that occurred from 1990-1992. Of these events, 77% involved stationary facilities and 23% were transportation-related. In 88% of events, a single chemical was released. The most commonly released hazardous substances were volatile organic compounds (18%), herbicides (15%), acids (14%), and ammonia (11%). These events resulted in 1,446 injuries and 11 deaths. Respiratory irritation (37%) and eye irritation (23%) were the most commonly reported symptoms. Chemical exposures also can occur at home or as the result of an attack.
Many common products once believed to be innocuous (eg, cement, gasoline) are now regarded as potentially hazardous and as the cause of serious injury and illness. Exposure to these agents can be reduced significantly through educational programs, cautionary labeling of toxic products, and appropriate use of protective clothing.
When poison control centers identify new products that are toxic to skin, information is added to the regional poison information system to ensure that injured patients are given the benefit of new data. Concomitantly, this information is shared with the manufacturer and Consumer Product Safety Commission (CPSC) to recognize and address the problem nationally. For example, numerous cases of serious permanent injury and, occasionally, death caused by exposure to sulfuric acid drain cleaners have been recorded by the CPSC. As a result of this alarming problem, the CPSC currently proposes banning the sale of this product to consumers.
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