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When ketones appear in the urine, they signify high levels of blood acids and ill-controlled diabetes. Urine showing ketones can be an alarming sign for people having diabetes requiring quick medical intervention.  Diabetic ketoacidosis is a severe complication arising out of high levels of blood acids (ketones). This leads to intoxication of the bloodstream causing diabetic ketoacidosis.  Excessive ketones can lead to poisoning of the body. Diabetic ketoacidosis can also case loss of consciousness, interfering with body’s metabolism. Ketones build up can also lead to abruptly changing fluid levels causing the lungs to fill up. When ketones reach dangerous levels in people suffering from diabetes, diabetic coma or even death can occur.  It is very important to check for ketones through examinations and warning signals.
People having diabetes or at risk for diabetes should be aware of the warning signs of diabetic ketoacidosis. During treatment, if blood sugar level is adjusted too quickly it can cause swelling in the brain.
Ketoacidosis, which generally develops slowly, can become a fatal condition within a matter of hours.  Attending it immediately is crucial for avoiding life-threatening conditions.
The most common symptoms of meningitis are headache and neck stiffness associated with fever, confusion or altered consciousness, vomiting, and an inability to tolerate light (photophobia) or loud noises (phonophobia). Nuchal rigidity occurs in 70% of adult cases of bacterial meningitis.[6] Other signs of meningism include the presence of positive Kernig's sign or Brudzinski's sign.
Meningitis caused by the bacterium Neisseria meningitidis (known as "meningococcal meningitis") can be differentiated from meningitis with other causes by a rapidly spreading petechial rash which may precede other symptoms.[7] The rash consists of numerous small, irregular purple or red spots ("petechiae") on the trunk, lower extremities, mucous membranes, conjuctiva, and (occasionally) the palms of the hands or soles of the feet. A severe case of meningococcal meningitis in which the petechial rash progressed to gangrene and required amputation of all limbs. People with meningitis may develop additional problems in the early stages of their illness.
The brain tissue may swell, with increasing pressure inside the skull and a risk of swollen brain tissue causing herniation. Recent trauma to the skull gives bacteria in the nasal cavity the potential to enter the meningeal space.
Recurrent bacterial meningitis may be caused by persisting anatomical defects, either congenital or acquired, or by disorders of the immune system.[14] Anatomical defects allow continuity between the external environment and the nervous system. The term aseptic meningitis refers loosely to all cases of meningitis in which no bacterial infection can be demonstrated.
A parasitic cause is often assumed when there is a predominance of eosinophils (a type of white blood cell) in the CSF. The meninges comprise three membranes that, together with the cerebrospinal fluid, enclose and protect the brain and spinal cord (the central nervous system).
In bacterial meningitis, bacteria reach the meninges by one of two main routes: through the bloodstream or through direct contact between the meninges and either the nasal cavity or the skin. The large-scale inflammation that occurs in the subarachnoid space during meningitis is not a direct result of bacterial infection but can rather largely be attributed to the response of the immune system to the entrance of bacteria into the central nervous system.
It is recognized that administration of antibiotics may initially worsen the process outlined above, by increasing the amount of bacterial cell membrane products released through the destruction of bacteria. In someone suspected of having meningitis, blood tests are performed for markers of inflammation (e.g. The most important test in identifying or ruling out meningitis is analysis of the cerebrospinal fluid through lumbar puncture (LP, spinal tap).[20] However, lumbar puncture is contraindicated if there is a mass in the brain (tumor or abscess) or the intracranial pressure (ICP) is elevated, as it may lead to brain herniation. A lumbar puncture is done by positioning the patient, usually lying on the side, applying local anesthetic, and inserting a needle into the dural sac (a sac around the spinal cord) to collect cerebrospinal fluid (CSF).
Various more specialized tests may be used to distinguish between various types of meningitis. A diagnostic and therapeutic conundrum is the "partially treated meningitis", where there are meningitis symptoms after receiving antibiotics (such as for presumptive sinusitis). Histopathology of bacterial meningitis: autopsy case of a patient with pneumococcal meningitis showing inflammatory infiltrates of the pia mater consisting of neutrophil granulocytes (inset, higher magnification).
For some causes of meningitis, prophylaxis can be provided in the long term with vaccine, or in the short term with antibiotics.
Since the 1980s, many countries have included immunization against Haemophilus influenzae type B in their routine childhood vaccination schemes. Short-term antibiotic prophylaxis is also a method of prevention, particularly of meningococcal meningitis. Mechanical ventilation may be needed if the level of consciousness is very low, or if there is evidence of respiratory failure. Structural formula of ceftriaxone, one of the third-generation cefalosporin antibiotics recommended for the initial treatment of bacterial meningitis.
Empiric antibiotics (treatment without exact diagnosis) must be started immediately, even before the results of the lumbar puncture and CSF analysis are known.
A 2010 analysis of previous studies has shown that the benefit from steroids may not be as significant as previously found. Viral meningitis typically requires supportive therapy only; most viruses responsible for causing meningitis are not amenable to specific treatment. In children there are several potential disabilities which result from damage to the nervous system. When ICP exerts enough pressure to displace a portion of the brain, herniation (an upward, downward, or lateral pushing of a portion of the brain through an opening) can occur. Herniation can also occur through a previous craniotomy site or through an opening caused by trauma. When ICP is elevated, an LP is contraindicated because the withdrawal of even a small amount of CSF can cause the brain to shift, or herniate.
After the original injury, a postconcussion syndrome may persist for several weeks to months.
A skull fracture may be open, closed, simple, depressed, or comminuted (fragmented), depending on whether the skull and scalp are intact. Open skull fractures potentially expose the brain to external microorganisms, which could lead to meningitis or encephalitis. In a basilar skull fracture, rhinorrhea, leakage of CSF from the nose (otorrhea), or leakage of CSF from the ear may occur. Figure 78-7 illustrates the effects of a basilar fracture with periorbital ecchymosis (raccoon’s eyes) and periauricular ecchymosis (Battle’s sign). An epidural hematoma is an accumulation of blood, usually from the temporal artery, between the dura and the skull (Fig. FIGURE 78-7 · (A) Basilar skull fracture in the temporal bone can cause cerebrospinal fluid (CSF) to leak from the nose or ear (B) Periorbital ecchymosis, called raccoon’s eyes.
An intracranial (intracerebral) hematoma is caused by hemorrhage and edema that results from bleeding within the skull (Fig. 11.Toussaint LG 3 rd , Friedman JA, Wijdicks EF, Piepgras DG, Pichelmann MA, McIver JI, et al.

The causes of dilated pupils are multiple, ranging from drugs, poisons, medications, or brain injury or disease. Therapeutic medications and some illicit drugs are all prone to cause the pupils to dilate. It is better to know the exact symptoms of dilated pupils, for it offers you more options to trace its causes. Surprisingly, some people may recognize their diabetes only due to diabetic ketoacidosis appearing as the first sign.
This is owing to insufficient insulin availability and can be more commonly observed in people suffering from type 1 diabetes. Since there is not sufficient insulin production, the body starts to rely on the alternate source of fuel – fat. This condition, called adult respiratory distress syndrome, can create serious breathing problems.
Diabetic ketoacidosis can be highest among people having type 1 diabetes,  those missing insulin too often and people younger than 19.
When there is a sudden (quick) drop in blood sugar level due to insulin administration, there can be incidence of hypoglycemia. The possibility of complications arising out of treating diabetic ketoacidosis are not common now, although they can prove to be concerning when they occur. Sometimes, especially in small children, only nonspecific symptoms may be present, such as irritability and drowsiness.
This involves inserting a needle into the spinal canal to extract a sample of cerebrospinal fluid (CSF), the fluid that envelops the brain and spinal cord.
Kernig's sign is assessed with the patient lying supine, with the hip and knee flexed to 90 degrees. The rash is typically non-blanching: the redness does not disappear when pressed with a finger or a glass tumbler. The patient, Charlotte Cleverley-Bisman, survived the disease and became a poster child for a meningitis vaccination campaign in New Zealand. These may require specific treatment, and sometimes indicate severe illness or worse prognosis. In premature babies and newborns up to three months old, common causes are group B streptococci (subtypes III which normally inhabit the vagina and are mainly a cause during the first week of life) and those that normally inhabit the digestive tract such as Escherichia coli (carrying K1 antigen). Similarly, individuals with a cerebral shunt or related device (such as an extraventricular drain or Ommaya reservoir) are at increased risk of infection through those devices. This is usually due to viruses, but it may be due to bacterial infection that has already been partially treated, with disappearance of the bacteria from the meninges, or by infection in a space adjacent to the meninges (e.g.
The pia mater is a very delicate impermeable membrane that firmly adheres to the surface of the brain, following all the minor contours.
In most cases, meningitis follows invasion of the bloodstream by organisms that live upon mucous surfaces such as the nasal cavity. When components of the bacterial cell membrane are identified by the immune cells of the brain (astrocytes and microglia), they respond by releasing large amounts of cytokines, hormone-like mediators that recruit other immune cells and stimulate other tissues to participate in an immune response. When this has been achieved, the "opening pressure" of the CSF is measured using a manometer.
In bacterial meningitis it is typically lower; the CSF glucose level is therefore divided by the blood glucose (CSF glucose to serum glucose ratio).
A latex agglutination test may be positive in meningitis caused by Streptococcus pneumoniae, Neisseria meningitidis, Haemophilus influenzae, Escherichia coli and group B streptococci; its routine use is not encouraged as it rarely leads to changes in treatment, but it may be used if other tests are not diagnostic. When this happens, CSF findings may resemble those of viral meningitis, but antibiotic treatment may need to be continued until there is definitive positive evidence of a viral cause (e.g. The findings from a post mortem are usually a widespread inflammation of the pia mater and arachnoid layers of the meninges covering the brain and spinal cord.
This has practically eliminated this pathogen as a cause of meningitis in young children in those countries.
In cases of meningococcal meningitis, prophylactic treatment of close contacts with antibiotics (e.g. The choice of initial treatment depends largely on the kind of bacteria that cause meningitis in a particular place. Herniation causes severe injury to the brain because of prolonged hypoxia to parts of the brain that control the vital functions of the body—breathing and blood circulation. The concussion may not damage any brain structures, but temporary unconsciousness is possible.
The brain may be hit on one side (coup) and then bounce (rebound) off the other side of the skull (contrecoup).
Symptoms include headache, anxiety, fatigue, or vertigo (a sensation of rotation of self or one’s surroundings; not true dizziness). Lacerations are commonly associated with depressed skull fractures, which are discussed below. The fracture breaks the bone and forces the broken edges to press against the brain, resulting in a significant risk for ClCP and meningitis. A basilar skull fracture is especially dangerous because of potential damage to the vital centers that control blood pressure and respiration. ECG changes in SAH may mimic myocardial infarction or ischemia, and thus lead to delayed treatment of the primary problem. Spontaneous subarachnoid hemorrhage as a differential diagnosis of pre-hospital cardiac arrest.
Survival of a subarachnoid hemorrhage patient who presented with prehospital cardiopulmonary arrest: Case report and review of the literature.
Spontaneous subarachnoid hemorrhage as a cause of out-of-hospital cardiac arrest: True or not? Subarachnoid hemorrhage as a cause of out-of-hospital cardiac arrest: A prospective computed tomography study.
A systemic evaluation of the effect of temperature on coagulation enzyme activity and platelet function. Complete recovery from aneurysmal subarachnoid hemorrhage associated with out-of-hospital cardiopulmonary arrest.
Management of subarachnoid hemorrhage patients who presented with respiratory arrest resuscitated with bystander CPR.
They appear as the black circles, or openings, to allow the eyes to pick up the lights coming through it, which in turn to be sensed by light-sensitive cells in the back of the eyes.
It is common for eyes to dilate when you find yourself in dark places trying to allow in more light, while your eyes may remain normal-sized in a well-lit room. Almost 50% of the diabetes-related hospitalizations (type 1 diabetes) can be accounted to this condition. The CSF is then examined in a medical laboratory.[3] The usual treatment for meningitis is the prompt application of antibiotics and sometimes antiviral drugs. The infection may trigger sepsis, a systemic inflammatory response syndrome of falling blood pressure, fast heart rate, high or abnormally low temperature and rapid breathing.

The arachnoid mater (so named because of its spider-web-like appearance) is a loosely fitting sac on top of the pia mater.
This is often in turn preceded by viral infections, which break down the normal barrier provided by the mucous surfaces. The blood-brain barrier becomes more permeable, leading to "vasogenic" cerebral edema (swelling of the brain due to fluid leakage from blood vessels).
Most of the antibiotics used in meningitis have not been tested directly on meningitis patients in clinical trials. With treatment, mortality (risk of death) from bacterial meningitis depends on the age of the patient and the underlying cause. The brain herniates (pushes) through the large foramen (opening) in the occipital bone, which lies between the cranial and spinal cavities. A positive test for CSF is known as a halo sign (see In Practice: Nursing Care Guidelines 78-3).
The cause may be rupture of delicate blood vessels owing to hypertension or a cerebral aneurysm. Early identification of SAH-induced cardiac arrest with the use of computed tomography scan of the brain obtained immediately after resuscitation will aid emergency physicians make further decisions. And the size of the opening is to be determined by the iris, known to be the colored part of the eye surrounding the pupil. A positive Brudzinski's sign occurs when flexion of the neck causes involuntary flexion of the knee and hip. Older children are more commonly affected by Neisseria meningitidis (meningococcus), Streptococcus pneumoniae (serotypes 6, 9, 14, 18 and 23) and those under five by Haemophilus influenzae type B (in countries that do not offer vaccination, see below).[1][3] In adults, N. Endocarditis (infection of the heart valves with spread of small clusters of bacteria through the bloodstream) may cause aseptic meningitis. The subarachnoid space separates the arachnoid and pia mater membranes, and is filled with cerebrospinal fluid. Once bacteria have entered the bloodstream, they enter the subarachnoid space in places where the blood-brain barrier is vulnerable—such as the choroid plexus.
Large numbers of white blood cells enter the CSF, causing inflammation of the meninges, and leading to "interstitial" edema (swelling due to fluid between the cells).
Thus, corticosteroids are recommended in the treatment of pediatric meningitis if the cause is H. Some clients recover from concussions with no apparent ill effects except the inability to remember the event; others have blurred vision or severe headaches. With direct and rebound trauma, blood vessels, nerve tracts, brain tissue, and other structures are bruised and torn. Any scalp lacerations must be thoroughly examined to determine if the cranium has been opened. If, for example, the bone fragment presses on the brain’s speech center, the client’s speech may be impaired until the pressure is relieved. Specific signs and symptoms are determined by the area of the brain affected and the extent of any neurologic damage. A high index of suspicion is required as the clinical presentation of cardiac arrest secondary to SAH can be obscure. The pupil dilation or dilated pupils come to occur when the size of it enlarges to allow in more light to the eye. Aseptic meningitis may also result from infection with spirochetes, a type of bacteria that includes Treponema pallidum (the cause of syphilis) and Borrelia burgdorferi (known for causing Lyme disease). The outermost membrane, the dura mater, is a thick durable membrane, which is attached to both the arachnoid membrane and the skull.
In addition, the walls of the blood vessels themselves become inflamed (cerebral vasculitis), which leads to a decreased blood flow and a third type of edema, "cytotoxic" edema. A client who has had anything other than a very minor concussion should see a physician immediately for a thorough neurologic examination. Usually, the person is unconscious immediately after the injury, lucid for a brief period, then unconscious again as blood accumulates in the epidural space and causes pressure.
But, prompt neurosurgical referral and multidisciplinary intensive care management can improve the survival rate and the functional outcome.
Thus, physicians should consider SAH as a differential diagnosis in patients presenting with pre-hospital cardiac arrest. Dilated pupils may be something inconsequent but sometimes caused by other severe problem it will beget trouble. When the emergency medical services arrived at the scene 15 minutes later, the initial cardiac rhythm was pulseless electrical activity (PEA).
There was no bystander CPR till then, and they immediately commenced CPR and inserted laryngeal mask airway.On arrival in the ED, the patient was still in PEA. He had an episode of ventricular tachycardia, and after a single episode of defibrillation, he regained spontaneous circulation. Serial post-resuscitation ECGs showed ST elevation in aVR and ST depression in other leads [Figure 1]. After discussion with the neurosurgeon, cardiologist, and intensive care physician, the patient was admitted to neurosurgical ICU for further management. It carries a high mortality rate of around 35-40% despite neurosurgical treatment advances.
The most common cause of SAH is rupture of an aneurysm in a blood vessel in the brain, but can also occur due to arterio-venous malformation or a traumatic event.About 10% of the patients with spontaneous SAH present to the emergency department (ED) with out-of-hospital cardiac arrest.
The mechanism of cardiac arrest secondary to SAH has been attributed to a sudden increase in intracranial pressure caused by massive SAH, which results in brainstem herniation leading to respiratory arrest.
SAH also leads to sympathetic hyperstimulation and release of cathecolamines, resulting in lethal cardiac arrhythmias and subsequent cardiac arrest. The pattern of large inverted T waves along with prolonged QTc is commonly known as "cerebral" T wave. SAH also predisposes the patients to all cardiac arrhythmias, especially malignant ventricular arrhythmias like ventricular tachycardia, ventricular fibrillation, and torsades de pointes. Thus, ECG changes in SAH may mimic myocardial infarction or ischemia, and thus lead to delayed treatment of the primary problem.PEA is found to be the initial cardiac rhythm in 44% of the SAH patients with cardiac arrest, with 48% having asystole and only 8% having ventricular fibrillation.
Moreover, post-resuscitation therapeutic hypothermia is unwarranted in patients with SAH as it would increase the bleeding tendency, which could prove to be detrimental. There have been reports of few cases who have survived the event, but the prognosis is poor. Some patients had complete neurological recovery, but most of them resulted in brain death, vegetative state or severe brain damage; and the chance of long term survival is small.
The overall prognosis of patients who are resuscitated is extremely poor with a low survival rate.

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