an injury cerebro-spinal fluid is found escaping from the skull, it proves that there is a laceration of the visceral layer of the arachnoid membrane communicating with 'a fracture of the bone. When the escape of this fluid is very abundant, and particularly if it flows from a fracture of the vault, it is accepted as evidence of a concussion or the brain opening up one of the veins. The cerebro-spinal fluid may escape from a wound in the soft parts, or form the cystic tumour of the scalp previously described (see p 73) ■ as a complication of fractures of the base it is a very rare circumstance. <Callout type="warning" title="Cerebro-Spinal Fluid Leak">Seek immediate medical attention if cerebro-spinal fluid is observed.</Callout> When after an injury to the head a patient is absolutely unconscious, it being impossible to arouse him or make him answer questions with sedation, 92 SURGICAL DIAGNOSIS [chap. dilated pupils, slow, deep, stertorous breathing with flapping of the cheeks during expiration, slow, full, laboured pulse, and paralysis, general or of one side of the body only, with exaggeration of the patellar reflex, at any rate on one side of the body opposite to the site of the compression — these symptoms are caused by compression of the brain. An attempt must be made to determine the source of the compression, and first of all depressed bone must be sought; and if a depressed fracture is detected, and the symptoms of compression are known to have been instantly produced, it may be regarded as the cause of the compression. If, however, the symptoms of compression have come on gradually and at a short interval after the accident (an interval during which the patient may have been quite conscious, or showing more or less evidence of brain concussion), or if while under observation it is noted that the signs of compression are increasing, the coma becoming more deep, the pupils changing from a condition of contraction to increasing dilatation, and the paralysis more extensive, it indicates intracranial hemorrhage. When there has been an interval of consciousness between the injury and the onset of the symptoms of compression, showing that the brain has not been seriously shaken or contused; and, further, if the paralysis is or was at first unilateral, we may diagnose that the hemorrhage has taken place between the bone and the dura mater from rupture of a meningeal artery or wound of a sinus. But if the symptoms point to severe immediate injury to the brain, it is probable that the blood-clot is situated on or in the brain. Symptoms of compression coming on after an interval of days or weeks from the injury, and preceded by signs of intracranial inflammation, indicate that the cause is the pressure of inflammatory products. {See p. 97.) In any case of compression the tension of the cerebro-spinal fluid is raised, as shown by the rate of flow from the needle, on lumbar puncture, being greater than normal. After a fracture of the base of the skull, or when laceration or arachnoid hemorrhage has occurred, the fluid may be stained with blood. When the history and symptoms indicate extra-meningeal hemorrhage the surgeon must determine on which side the clot of blood is. Five signs will guide him. (a) If there is paralysis on one side only, or the paralysis is more marked on one side than the other, or the general paralysis has been preceded by unilateral spasm, the blood-clot is on the side opposite to the paralysis or spasm, {b) The hemorrhage will be on the same side of the skull as the injury; and therefore if a bruise can be detected on one side, or if there is a wound, this will guide the surgeon as to the position of the clot. (c) If one pupil only is dilated, the clot is on the same side as the paralyzed pupil, {d) If one patellar reflex is brisker than its fellow, the clot is on the opposite side to the brisk reflex, (e) If the temperature is found to be different on the two sides of the body, the clot will be found on the side opposite to the higher temperature. The symptoms of intracranial hemorrhage are often mixed with and obscured by those of severe concussion and laceration of the brain; they are mainly characterized by paralytic phenomena. If the surgeon should trephine the skull in the supposition that there is a clot of blood between the bone and the dura mater, and on removing the piece of bone fails to find the clot, but notices that the untorn dura mater bulges up into the trephine hole, and is pulseless, and 'of dark-blue colour, he may diagnose arachnoid hemorrhage, and should make an incision into the dura mater. 7. Cases often present themselves in which there is great difficulty in determining whether the symptoms are due to the effects of alcohol or to a serious lesion of the brain. Whenever there is this doubt and whenever a drunken man is known to have received a severe injury to the head, he should be kept quiet for some hours until the effects of the alcohol have passed off. The signs of alcoholism upon which reliance is generally placed are the peculiar odour of the breath, the flushed face, heavy but not stertorous breathing, the contracted pupils, which dilate on arousing the patient, incoherent delirium, a tendency to become quarrelsome, tremor and unsteadiness of gait if able to walk at all, the absence of paralysis, and finding the bladder full of urine, in which alcohol may sometimes be detected. _ The history, where obtainable, is of course of the highest importance. 8. In other instances the question arises whether a person found insensible and paralysed has had an attack of apoplexy, and fallen down, or has received a serious head injury causing the paralysis. Here again there are cases in which it may be necessary to suspend judgment for a time, or even altogether. For the symptoms produced by a clot of blood in the brain are of course the same whether the rupture of the blood-vessel be spontaneous or be excited by a blow In all such cases the age of the patient and all the attendant circumstances must be carefully noted, and the heart and the urine should be examined, as the detection of a cardiac murmur or of an aortic aneurysm, or of albuminuria, would be strong corroboration of the diagnosis of apoplexy. Careful search should be made for a wound or contusion of the scalp, depression of bone, bleeding from the nose, ear, or pharynx. A disproportion between the loss of consciousness and the paralysis, if present, would be of great assistance in the diagnosis, for in traumatic cases the sensorium, as a rule, suffers much more than the motorium, while in the idiopathic cases there may be complete hemiplegia with only very transient insensibility. 9. Diabetic coma may in rare cases need to be distinguished from traumatic unconsciousness. The presence of sugar in the urine, the odour of acetone in the breath, the deep coma without paralysis, the flushed face, rapid deep respirations with rapid weak pulse, will establish the diagnosis. With regard to lesions of cranial nerves the following points are of practical importance : Loss of smell is the indication of injury to the olfactory nerve; but care must be taken to ascertain that the nasal fossa is clear, and not obstructed by blood-clot, dried discharge, displaced bone or cartilage. The optic nerve may be injured in the optic foramen by a fracture of the anterior fossa of the skull, or by a blow upon the outer wall of the orbit; the result is blindness of one eye. Injury of the 3rd nerve (mrvus oculo-motorius) often affects only a part of the nerve ; thus a common occurrence is ptosis, external strabismus with inability to move the globe upwards, downwards or inwards, a fixed dilated pupil and loss of power of accommodation, so that the patient has horizontal diplopia with one clear and one blurred image indicate complete paralysis of the 3rd nerve. Paralysis of the superior oblique muscle causing diplopia below the horizontal meridian, and internal strabismus when the eyeball is directed downwards, may indicate a lesion of the 4th nerve (nervus trochleae), or of its centre, or interference with the play of the tendon of the muscle in its pulley; any thickening, pain, or tenderness at the seat of the pulley would render the latter the more probable diagnosis. The 5th nerve (nervus trigeminus) is rarely affected alone ; when the lesion is partial the cornea rapidly sloughs unless protected. Internal strabismus without palsy of any muscle except the external rectus points to injury of the 6th cranial nerve (nervus abducens) alone. The 7th nerve (nervus facialis) is the one most frequently injured in fracture of the skull ; the signs of facial palsy are unmistakable. In estimating deafness from injury to the 8th nerve (nervus acusticus), reliance must be placed upon failure to appreciate sounds transmitted through the cranial bones rather than those transmitted through the auditory meatus and tympanum, as these may be obstructed by a clot of blood in the 9th, 10th, and Uth nerves (nervi glossopharyngeus, vagus, and hypoglossus). Injury to the 9th nerve results in difficulty in swallowing and loss of taste over the back of the tongue. — Loss of cardiac rhythm and aid of the cervical part of the vagus. The 12th nerve (nervus hypoglossus) may be injured in fractures of the posterior fossa, resulting in deviation of the protruded tongue towards the injured side, and, later, wasting of this side of the tongue. Secondary complications of intracranial injuries. — These complications are — Spreading edema of the brain. Leptomeningitis. Subdural suppuration. Hernia cerebri. Traumatic neurasthenia. When a patient recovering from the symptoms of cerebral concussion relapses into unconsciousness with rapidly increasing muscular weakness and paralysis, frequent weak pulse, high temperature, and coma fatal in a few hours, the cause of the symptoms is spreading edema of the brain. The same symptoms may occur during reaction in cases of cerebral contusion, and after the removal of a large extradural clot, where the sudden relief of pressure upon the brain is followed by hyperaemia and hemorrhage into the cortex. The rapid onset of coma in some cases of cerebral tumour is due to the same cause. 2. When after a head injury there are headache with high fever— perhaps ushered in by a rigor— vomiting, and a rapid full pulse, and these symptoms pass in a few hours into a condition of great restlessness, excitement or delirium, with intolerance of light and sound, small pupils, optic neuritis, muscular twitchings or convulsions, and then paralysis, and these symptoms again rapidly pass into a condition of increasing drowsiness and weakness ending in coma with fixed dilated pupils, rapid feeble pulse and irregular or Cheyne-Stokes stertorous breathing the cause of these symptoms is diffuse leptomeningitis or meningocerebritis. The presence of retraction of the head and of intense optic neuritis, and the early and frequent occurrence of convulsion, points to a basal meningitis; and if the convulsions are limited in area this diagnosis is clearer. The symptoms of this disease vary greatly; those lost constant are headache, progressive paralysis, and coma. Examination of the eye does not show tubercles in the choroid, lumbar puncture will demonstrate increased tension of the cerebro-spinal fluid. Cytological examination of the fluid withdrawn will yield an increased cellular content or even a definite admixture of pus. If after an injury to the vault of the skull there are persistent local pain and tenderness, pachymeningeal thickening may be diagnosed; and if there is a purplish swell- ing of the scalp over the injured part with signs of localized compression of the cortex-localized jasms followed by paralysis—this would be evidence of an abscess. The bone should be trephined and pus may be found between it and the dura mater; if not and the membranes bulge into the trephine hole and show no pulsation, an incision should be made through the dura mater and a sample of a subdural abscess let out. 6. The symptoms of cerebral abscess are very am- biguous: persistent subnormal increasing drowsiness, optic neuritis, and headache after a head injury there is fever, perhaps ushered in by a rigor— vomiting, and a rapid full pulse, and these symptoms pass in a few hours into a condition of great restlessness, excitement or delirium, with intolerance of light and sound, small pupils, optic neuritis, muscular twitchings or convulsions, and then paralysis, and these symptoms again rapidly pass into a condition of increasing drowsiness and weakness ending in coma with fixed dilated pupils, rapid feeble pulse and irregular or Cheyne-Stokes stertorous breathing. The history of injury to the bone preceding the appearance of the fungus at once distinguishes it from pulsating malignant tumour. Where the hernia is of small size and slow growth a small abscess will almost certainly be found beneath it, and is its cause. But where the hernia is of large size and rapidly enlarging, it results from a diffuse leptomeningitis. Other and more chronic sequelae are glycosuria, diabetes insipidus, epilepsy, dementia, loss of memory, increased susceptibility to the intoxicating effect of alcohol, and deafness, amaurosis, anosmia, etc., where there has been cranial nerve injury. A frequent condition is traumatic neurasthenia, characterized by headache, inability to work, giddiness, tremors, loss of emotional control, flushing of the face and head, rapid pulse, sweating, increased knee-jerks and loss of weight. <Callout type="important" title="Cranial Nerve Injury">Identifying specific cranial nerve injuries is crucial for proper treatment.</Callout> <Callout type="risk" title="Intracranial Hemorrhage">Failure to diagnose or treat intracranial hemorrhage can lead to severe complications and death.</Callout>
Key Takeaways
- Identify cerebro-spinal fluid leaks as evidence of brain injury.
- Recognize signs of intracranial compression, such as dilated pupils and labored breathing.
- Use the five signs to determine the location of a blood clot in cases of extra-meningeal hemorrhage.
Practical Tips
- Always seek immediate medical attention for suspected head injuries, especially if cerebro-spinal fluid is observed leaking from the skull.
- Be aware that alcohol can mimic symptoms of brain injury and delay proper diagnosis and treatment.
- Carefully examine the patient's history to determine whether a traumatic event or an idiopathic condition caused their symptoms.
Warnings & Risks
- Failure to diagnose intracranial hemorrhage can lead to severe complications and death.
- Incorrectly attributing symptoms to alcohol instead of brain injury can delay necessary medical intervention.
- Ignoring the signs of cranial nerve injury may result in improper treatment or misdiagnosis.
Modern Application
While many of the techniques described in this chapter are outdated, the principles of recognizing and responding to head injuries remain crucial for modern survival preparedness. Understanding how to identify cerebro-spinal fluid leaks and intracranial hemorrhages can save lives in emergency situations where immediate medical care may not be available.
Frequently Asked Questions
Q: How can you tell if a patient is experiencing an intracranial hemorrhage?
Look for signs such as unconsciousness, dilated pupils, labored breathing, and paralysis. These symptoms often indicate compression of the brain, which may be caused by an intracranial hemorrhage.
Q: What should you do if cerebro-spinal fluid is observed leaking from a patient's skull?
Seek immediate medical attention as this can indicate a serious injury and requires prompt treatment to prevent complications.
Q: How can alcohol affect the diagnosis of head injuries?
Alcohol can mimic symptoms of brain injury, such as confusion and dizziness. It is important to consider the patient's history and behavior to differentiate between alcohol-induced effects and actual brain damage.